Mirdametinib (PD0325901) is an orally active, selective and non-ATP-competitive MEK inhibitor with an IC50 of 0.33 nM. Mirdametinib exhibits a Kiapp of 1 nM against activated MEK1 and MEK2. Mirdametinib suppresses the expression of p-ERK1/2 and induces apoptosis. Mirdametinib has anti-cancer activity for a broad spectrum of human tumor xenografts .
Ulixertinib (BVD-523; VRT752271) is a potent, orally active, highly selective, ATP-competitive and reversible covalent inhibitor of ERK1/2 kinases, with an IC50 of <0.3 nM against ERK2. Ulixertinib (BVD-523; VRT752271) inhibits the phosphorylated ERK2 (pERK) and downstream kinase RSK (pRSK) in an A375 melanoma cell line .
AMG PERK 44 is an orally active and highly selective PERK inhibitor with an IC50 of 6 nM. AMG PERK 44 has 1000-fold and 160-fold selectivity over GCN2 (IC50=7300 nM) and B-Raf (IC50 >1000 nM), respectively. AMG PERK 44 induces autophagy .
Bufotalin is a steroid lactone isolated from Venenum Bufonis with potently antitumor activities. Bufotalin induces cancer cell apoptosis and also induces endoplasmic reticulum (ER) stress activation .
Ulixertinib hydrochloride (BVD-523 hydrochloride) is a potent, orally active, highly selective, ATP-competitive and reversible covalent inhibitor of ERK1/2 kinases, with an IC50 of <0.3 nM against ERK2. Ulixertinib hydrochloride inhibits the phosphorylated ERK2 (pERK) and downstream kinase RSK (pRSK) in an A375 melanoma cell line .
GSK621 is a specific AMPK activator, with IC50 values of 13-30 μM for AML cells. GSK621 induces autophagy and apoptosis. GSK621 induces eiF2α phosphorylation-a hallmark of UPR activation .
Milnacipran hydrochloride is an orally active Serotonin (HY-B1473A) and Norepinephrine (HY-13715) reuptake inhibitor. Milnacipran hydrochloride inhibits monoamine transporters, especially the norepinephrine transporter and the serotonin transporter (Ki values of 31 and 8.5 nM, respectively). Milnacipran hydrochloride inhibits pERK1/2 activation. Milnacipran hydrochloride has antidepressant, anxiolytic and analgesic properties. Milnacipran hydrochloride inhibits biting behavior in mice. Milnacipran hydrochloride can be used in the study of major depressive disorder, anxiety disorders, and neuropathic pain (e.g., fibromyalgia) .
Trametiglue, a derivative of Trametinib (HY-10999), targets both KSR-MEK and RAF-MEK with unprecedented potency and selectivity via unique interfacial binding interactions .
Ro 67-7476 is a potent positive allosteric modulator of mGluR1 and potentiates glutamate-induced calcium release in HEK293 cells expressing rat mGluR1a with an EC50 of 60.1 nM . Ro 67-7476 is a potent P-ERK1/2 agonist and activates ERK1/2 phosphorylation in the absence of exogenously added glutamate (EC50=163.3 nM) .
BAY 2965501 is a potent and selective diacylglycerol kinase zeta (DGKζ) inhibitor. BAY 2965501 induces pERK activation. BAY 2965501 can be used for the research of cancer .
Sulforaphene, isolated from radish seeds, exhibits an ED50 against velvetleaf seedlings approximately 2 x 10 -4 M. Sulforaphene promotes cancer cells apoptosis and inhibits migration via inhibiting EGFR, p-ERK1/2, NF‐κB and other signals .
IACS-13909 is a selective, potent and orally active SHP2 allosteric inhibitor with an IC50 of 15.7 nM and a Kd of 32 nM. IACS-13909 is more selective for SHP2 than other phosphatases (including SHP1). IACS-13909 has antitumor activities and suppresses MAPK pathway signaling in receptor tyrosine kinases (RTK)-dependent cancers .
1,2,4-Trihydroxybenzene (Hydroxyhydroquinone) is an ER stress inducer that targets proteins such as PKR-like ER kinase PERK to induce cytotoxicity. 1,2,4-Trihydroxybenzene selectively activates eIF2α phosphorylation, activates the PERK-eIF2α signaling pathway and induces stress granule formation. 1,2,4-Trihydroxybenzene subsequently exacerbates oxidative stress and causes DNA double-strand breaks, destroying organelles such as mitochondria and ER, and inducing cell death. 1,2,4-Trihydroxybenzene also has the potential to exhibit anti-tumor effect, increase blood pressure, and relieve spasm .
Vindoline is an orally active vinca alkaloid. Vindoline can be extracted from the leaves of Catharanthus roseus. Vindoline has a weak inhibitory effect on the self-assembly of tubulin. Vindoline alleviates Apoptosis, inhibits p-p65 and p-ERK. Vindoline improves diabetes, bone loss, osteoarthritis, and kidney damage .
ML417 is a selective and brain penetrant D3 dopamine receptor (D3R) agonist, with an EC50 of 38 nM. ML417 potently promotes D3R-mediated β-arrestin translocation, G protein mediated signaling, and pERK phosphorylation with minimal effects on other GPCR-mediated signaling. ML417 exhibits neuroprotection against toxin-induced neurodegeneration of dopaminergic neurons .
HC-5404-Fu is an orally active PERK inhibitor with an IC50 of 0.001 μM against human PERK. HC-5404-Fu blocks PERK activation induced by VEGFR-TKI and disrupts the adaptive stress response triggered by VEGFR-TKI. HC-5404-Fu enhances anti-angiogenic effects by inhibiting newly formed and mature tumor blood vessels in renal cell carcinoma models. HC-5404-Fu can be used in research related to renal cell carcinoma .
PROTAC K-Ras Degrader-5 is a cereblon-based K-Ras PROTAC degrader with a DC50 of <100 nM for KRAS G12D. PROTAC K-Ras Degrader-5 recruits KRAS G12D to the cereblon E3 ubiquitin ligase complex for ubiquitination and subsequent proteasomal degradation. PROTAC K-Ras Degrader-5 suppresses pERK levels downstream of KRAS G12D degradation in cancer cells. PROTAC K-Ras Degrader-5 reduces proliferation of cancer cells. PROTAC K-Ras Degrader-5 induces caspase 3/7 activity and cPARP, markers of apoptosis, in pancreatic cancer spheroids and tumors. PROTAC K-Ras Degrader-5 can be used for the research of pancreatic cancer and colorectal cancer .
Nedometinib (NFX-179) is a specific MEK1 inhibitor with an IC50 of 135 nM. Nedometinib inhibits p-ERK, MAPK. Nedometinib exerts anticancer activity against squamous cell carcinoma. Nedometinib can be used for research in dermatosis, neurofibromatosis .
TH-Z827 is a mutant selective KRAS(G12D) inhibitor with an IC50 of 2.4 μM. TH-Z827 does not bind KRAS(WT) or KRAS(G12C). TH-Z827 blocked the KRAS(G12D)-CRAF interaction with an IC50 value of 42 μM .
Claturafenib ( PF-07799933) is an orally active inhibitor of pan-mutant BRAF. Claturafenib inhibits pERK in cells (IC50 value of 1.6 nM in HT29 cells). Claturafenib has anticancer activity against BRAF G469A mutant NSCLC and BRAF K601E mutant melanoma .
PERK-IN-4 is a potent and selective PERK (protein kinase R (PKR)-like endoplasmic reticulum kinase) inhibitor with an IC 50 of 0.3 nM. PERK is activated in response to a variety of endoplasmic reticulum stresses implicated in numerous disease states .
MAP855 is a highly potent, selective, ATP-competitive and orally active MEK1/2 kinase inhibitor (MEK1 ERK2 cascade IC50=3 nM, pERKEC50=5 nM). MAP855 shows equipotent inhibition of wild-type and mutant MEK1/2 .
MSU-42011 is an orally active retinoid X receptor (RXR) agonist. MSU-42011 inhibits the iNOS activity and reduces the expression of p-ERK protein. MSU-42011 has immunomodulatory and antitumor activity .
RAS/RAS-RAF-IN-1 is a potent RAS and RAS-RAF inhibitor. RAS/RAS-RAF-IN-1 has a KD of 5.0 μΜ-15 μΜ for cyclophilin A (CYPA) binding affinity. RAS/RAS-RAF-IN-1 has antitumor activity .
(S)-BAY 2965501 is the left-handed isomer of BAY 2965501 (HY-153343). BAY 2965501 is a potent and selective diacylglycerol kinase zeta (DGKζ) inhibitor. BAY 2965501 induces pERK activation. BAY 2965501 can be used for the research of cancer .
ML291 is a UPR (unfolded protein response)-inducing sulfonamidebenzamide. ML291 overwhelms the adaptive capacity of the UPR and induces apoptosis in a variety of solid cancer models. ML291 can activate the PERK/eIF2a/CHOP (apoptotic) arm of the UPR and reduce leukemic cell burden .
GSK143 dihydrochloride is an orally active and highly selective spleen tyrosine kinase (SYK) inhibitor with a pIC50 of 7.5. GSK143 dihydrochloride inhibits phosphorylated Erk (pErk: pIC50=7.1) . GSK143 dihydrochloride reduces inflammation and prevents recruitment of immune cells in the intestinal muscularis in mice .
PERK/eIF2α activator 1 (compound V8) is a flavonoid with an anti-tumor activity. PERK/eIF2α activator 1 induces apoptosis and activates the PERK-eIF2α-ATF4 pathway. PERK/eIF2α activator 1 inhibits HepG2 cell proliferation with an IC50 value of 23 μM .
BTX-7312 is a cereblon-based SOS1 bifunctional degrader and a molecular glue. BTX-7312 reduces downstream signaling markers pERK and pS6 and shows antiproliferative activity in various KRAS-mutated cells .
PERK-IN-5 is a highly potent, selectively and orally bioavailable PERK inhibitor (IC50s of 2 and 9 nM for PERK and p-eIF2α, respectively). PERK-IN-5 can significantly inhibit tumor growth in the 786-O renal cell carcinoma xenograft tumor model .
Milnacipran is an orally active Serotonin (HY-B1473A) and Norepinephrine (HY-13715) reuptake inhibitor. Milnacipran inhibits monoamine transporters, especially the norepinephrine transporter and the serotonin transporter (Ki values of 31 and 8.5 nM, respectively). Milnacipran inhibits pERK1/2 activation. Milnacipran has antidepressant, anxiolytic and analgesic properties. Milnacipran inhibits biting behavior in mice. Milnacipran can be used in the study of major depressive disorder, anxiety disorders, and neuropathic pain (e.g., fibromyalgia) .
FGF7p is a small molecule peptide and a potential bladder protector. FGF7p can activate downstream signaling pathways of FGFR2 in the urinary tract epithelium (pFRS2α, pAKT and pERK). FGF7p alleviates cyclophosphamide induced apoptosis and tissue damage in urinary tract epithelial cells by activating AKT and its downstream anti apoptotic targets (pBAD, pS6/mTORC1). FGF7p is commonly used in the study of inflammatory conditions .
BTX-6654 formate is a target-dependent and -specific cereblon-based bifunctional SOS1 PROTAC degrader. BTX-6654 formate reduces downstream signaling markers pERK and pS6, and displays antiproliferative activity in cells harboring various KRAS mutations .
Dosimertinib-d5 (mesylate) is a potent and orally active EGFR inhibitor. Dosimertinib-d5 (mesylate) decreases the expression of p-EGFR and p-ERK protein levels. Dosimertinib-d5 (mesylate) shows antiproliferative and anti-tumor activity. Dosimertinib-d5 (mesylate) has the potential for the research of non-small-cell lung cancer (NSCLC) .
(4S)-PROTAC SOS1 degrader-1 (diTFA) is a potent PROTAC SOS1 degrader. (4S)-PROTAC SOS1 degrader-1 (diTFA) decreases the expression of pERK and RAS-GTP level in a dose-dependent manner. (4S)-PROTAC SOS1 degrader-1 (diTFA) significantly inhibits the tumor growth in vivo .
SHP244 is a conformational inhibitor targeting the "latch allosteric site" (site 2) of the SHP2 protein with an IC50 value for SHP2 WT of 60 μM. SHP244 has no significant effect on the level of p-ERK alone. SHP244 combined with RMC-4550 (HY-116009) ("tunnel site" site 1 inhibitor) can reduce p-ERK and inhibit the rebound of p-ERK, thereby reducing drug resistance. SHP244 can be used to study drug resistance in FGFR-driven cancers .
Isogosferol ((+)-Isogospherol; Isogospherol) is a potent anti-inflammatory agent. Isogosferol decreases LPS (HY-D1056)-stimulated NO and IL-1β expression. Isogosferol decreases the LPS (HY-D1056)-stimulated expression of iNOS, COX-2, NF-κB, and pERK1/2 .
BTX-6654 is a target-dependent and -specific cereblon-based bifunctional SOS1PROTAC degrader. BTX-6654 reduces downstream signaling markers pERK and pS6, and displays antiproliferative activity in cells harboring various KRAS mutations .
GSK143 is an orally active and highly selective spleen tyrosine kinase (SYK) inhibitor with a pIC50 of 7.5. GSK143 inhibits phosphorylated Erk (pErk: pIC50=7.1) . GSK143 reduces inflammation and prevents recruitment of immune cells in the intestinal muscularis in mice .
SDUY038 is a SHP2 allosteric inhibitor, with an IC50 of 1.2 μM and KD of 0.29 μM, respectively. SDUY038 exhibits pan-antitumor activity (IC50 = 7-24 μM) by suppressing pERK expression. SDUY038 exhibits t1/2 of 3.95 h by oral administration .
(4S)-PROTAC SOS1 degrader-1 is a potent PROTAC SOS1 degrader. (4S)-PROTAC SOS1 degrader-1 decreases the expression of pERK and RAS-GTP level in a dose-dependent manner. (4S)-PROTAC SOS1 degrader-1 significantly inhibits the tumor growth in vivo .
BS148 is a selective sigma-2 receptor (S2R) agonist with a Ki 20 nM. BS148 shows >80-fold selective for S2R than S1R. BS148 activates the endoplasmic reticulum stress response through the upregulation of protein kinase R-like ER kinase (PERK), activating transcription factor 4 (ATF4) genes, and C/EBP homologous protein (CHOP). BS148 induces apoptosis in melanoma cell. BS148 downregulates genes related to the cholesterol pathway and activates the MAPK signaling pathway. BS148 can be used for the study of melanoma .
HDAC-IN-50 is a potent and orally active FGFR and HDAC dual inhibitor with IC50 values of 0.18, 1.2, 0.46, 1.4, 1.3, 1.6, 2.6, 13 nM for FGFR1, FGFR2, FGFR3, FGFR4, HDAC1, HDAC2, HDAC6, HDAC8, respectively. HDAC-IN-50 induces Apoptosis and cell cycle arrest at G0/G1 phase. HDAC-IN-50 decreases the expression of pFGFR1, pERK, pSTAT3. HDAC-IN-50 shows anti-tumor activity .
VU0424465 is a potent and partial PAM (positive allosteric modulator)-agonist for mGlu5 mediated iCa 2+ mobilization. VU0424465 exhibits high affinity at MPEP allosteric binding site, with a Ki value of 11.8 nM. VU0424465 is also a agonist for pERK1/2 in cortical neurons .
Milnacipran-d10 (hydrochloride) is the deuterium labeled Milnacipran hydrochloride (HY-B0168A). Milnacipran hydrochloride is an orally active Serotonin (HY-B1473A) and Norepinephrine (HY-13715) reuptake inhibitor. Milnacipran hydrochloride inhibits monoamine transporters, especially the norepinephrine transporter and the serotonin transporter (Ki values of 31 and 8.5 nM, respectively). Milnacipran hydrochloride inhibits pERK1/2 activation. Milnacipran hydrochloride has antidepressant, anxiolytic and analgesic properties. Milnacipran hydrochloride inhibits biting behavior in mice. Milnacipran hydrochloride can be used in the study of major depressive disorder, anxiety disorders, and neuropathic pain (e.g., fibromyalgia) .
KRAS ligand 4 (compound 2) is a bifunctional molecular glue degrader based on SOS1. KRAS ligand 4 reduces downstream signaling markers pERK and pS6 and displays anti-additional activity in cells with multiple KRAS mutations .
Sulforaphene, isolated from radish seeds, exhibits an ED50 against velvetleaf seedlings approximately 2 x 10-4 M. Sulforaphene promotes cancer cells apoptosis and inhibits migration via inhibiting EGFR, p-ERK1/2, NF‐κB and other signals .
Teverelix (EP 24332) is a GnRH antagonist. Teverelix binds competitively and reversibly to GnRH receptors, thereby suppressing the release of LH and FSH. Teverelix can be used in the research of prostatic hyperplasia, endometriosis, and prostate cancer .
KRAS inhibitor-13 (compound 5-6) is a potent KRAS G12C inhibitor with an IC50 of 0.883 µM. KRAS inhibitor-13 shows p-ERK inhibition activities with IC50s of 5.9, >100 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-13 has the potential for the research of pancreatic, colorectal, and lung cancers .
PERK-IN-4-d3 is the deuterium labeled PERK-IN-4. PERK-IN-4 is a potent and selective PERK (protein kinase R (PKR)-like endoplasmic reticulum kinase) inhibitor with an IC50 of 0.3 nM. PERK is activated in response to a variety of endoplasmic reticulum stresses implicated in numerous disease states .
MEK-IN-5 is a potent MEK inhibitor and NO donor. MEK-IN-5 significantly reduces the levels of pMEK and pERK in a dose-dependent and time-dependent manner. MEK-IN-5 induces apoptosis in MDA-MB-231 cells .
Eif2ak3 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Eif2ak3 gene (Mouse), as well as a negative control, a positive control, and a FAM-labeled negative control.
EIF2AK3 Human Pre-designed siRNA Set A contains three designed siRNAs for EIF2AK3 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
Lamp1 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Lamp1 gene (Mouse), as well as a negative control, a positive control, and a FAM-labeled negative control.
CNBCA is a potent, selective, competitive SHP2 enzyme inhibitor, with the IC50 of 0.87 μM. CNBCA binds to full-length SHP2 and inhibits enzyme activity. CNBCA inhibits pAkt and pERK1/2, and the cell growth of BT474 and MDA-MB468 cells. CNBCA can be used for breast cancer study .
Antiproliferative agent-23 is a microtubule-destabilizing agent (MDA) and efficiently disturbes the tubulin-microtubule system. Antiproliferative agent-23 induces apoptosis via a mitochondrion-dependent pathway by downregulating the Bcl-2 protein, upregulating Bax and Cyt c proteins, and activating the caspase cascade. Antiproliferative agent-23 initiates reactive oxygen species (ROS)-mediated endoplasmic reticulum stress in A549/CDDP cells (cisplatin resistant cancer cell line) via the PERK/ATF4/CHOP signaling pathway. Antiproliferative agent-23 has anti-tumor activity .
EGFR-IN-154 (compound 4c) is an EGFR inhibitor with EC50 values of 0.16 μM, 21.73 μM and 41.56 μM against EGFR Del19, EGFR WT and EGFR L858R, respectively. EGFR-IN-154 shows anticancer activity on various cance cell lines. EGFR-IN-154 induces mitochondrial apoptosis, and decreases pERK1/2 and pAkt levels, but increases pJNK and pp38 levels .
BTK-IN-34 (compound 9h) is a selective BTK inhibitor. BTK-IN-34 shows antiproliferative activity in RAMOS cells through selective inhibition of pBTK (Tyr223) without affecting Lyn and Syk, upstream proteins in the BCR signaling pathway .
SOS1-IN-12 is a potent son of sevenless homolog 1 (SOS1) inhibitor with a Ki of 0.11 nM for SOS1 and an IC50 of 47 nM for pERK. SOS1-IN-13 can be used for researching anticancer .
Milnacipran-d5 hydrochloride is deuterium labeled Milnacipran hydrochloride (HY-B0168A). Milnacipran hydrochloride is an orally active Serotonin (HY-B1473A) and Norepinephrine (HY-13715) reuptake inhibitor. Milnacipran hydrochloride inhibits monoamine transporters, especially the norepinephrine transporter and the serotonin transporter (Ki values of 31 and 8.5 nM, respectively). Milnacipran hydrochloride inhibits pERK1/2 activation. Milnacipran hydrochloride has antidepressant, anxiolytic and analgesic properties. Milnacipran hydrochloride inhibits biting behavior in mice. Milnacipran hydrochloride can be used in the study of major depressive disorder, anxiety disorders, and neuropathic pain (e.g., fibromyalgia) .
Bufotalin is a steroid lactone isolated from Venenum Bufonis with potently antitumor activities. Bufotalin induces cancer cell apoptosis and also induces endoplasmic reticulum (ER) stress activation .
Milnacipran (hydrochloride) (Standard) is the analytical standard of Milnacipran hydrochloride (HY-B0168A). This product is intended for research and analytical applications. Milnacipran hydrochloride is an orally active Serotonin (HY-B1473A) and Norepinephrine (HY-13715) reuptake inhibitor. Milnacipran hydrochloride inhibits monoamine transporters, especially the norepinephrine transporter and the serotonin transporter (Ki values of 31 and 8.5 nM, respectively). Milnacipran hydrochloride inhibits pERK1/2 activation. Milnacipran hydrochloride has antidepressant, anxiolytic and analgesic properties. Milnacipran hydrochloride inhibits biting behavior in mice. Milnacipran hydrochloride can be used in the study of major depressive disorder, anxiety disorders, and neuropathic pain (e.g., fibromyalgia) .
SOS1-IN-13 is a potent son of sevenless homolog 1 (SOS1) inhibitor with IC50s of 6.5 nM and 327 nM for SOS1 and pERK, respectively. SOS1-IN-13 can be used for researching anticancer .
MT477 is a potent protein kinase C (PKC) inhibitor. MT477 induces apoptosis and necrosis. MT477 decreases the protein expression of Ras-GTP, p-Erk1/2, p-Elk1. MT477 shows antitumor activity .
Takeda-6D (compound 6d) is an orally active and potent BRAF/VEGFR2 inhibitor, with IC50 values of 7.0 and 2.2 nM, respectively. Takeda-6D shows antiangiogenesis by suppressing the VEGFR2 pathway in 293/KDR and VEGF-stimulated HUVEC cells.Takeda-6D shows significant suppression of ERK1/2 phosphorylation. Takeda-6D shows antitumor activity .
CB2 receptor agonist 3 is a robust and selective CB2 cannabinoid agonist with Kis of 7.6 and 900 nM for CB2 and CB1, respectively. CB2 receptor agonist 3 significantly increases P-ERK 1/2 expression in HL-60 cells .
TK-684 is a potent and selective allosteric SHP2 inhibitor with IC50 values of 2.1, ＞1000 nM for SHP2 WT, SHP22 PTP, respectively. TK-684 inhibits cell proliferation and induces apoptosis. TK-684 decreases the protein expression of p-AKT, p-ERK .
1,2,4-Trihydroxybenzene (Hydroxyhydroquinone) (Standard) is the analytical standard of 1,2,4-Trihydroxybenzene (HY-W010451). This product is intended for research and analytical applications. 1,2,4-Trihydroxybenzene (Hydroxyhydroquinone) is an ER stress inducer that targets proteins such as PKR-like ER kinase PERK to induce cytotoxicity. 1,2,4-Trihydroxybenzene selectively activates eIF2α phosphorylation, activates the PERK-eIF2α signaling pathway and induces stress granule formation. 1,2,4-Trihydroxybenzene subsequently exacerbates oxidative stress and causes DNA double-strand breaks, destroying organelles such as mitochondria and ER, and inducing cell death. 1,2,4-Trihydroxybenzene also has the potential to exhibit anti-tumor effect, increase blood pressure, and relieve spasm .
SHP2-IN-31 is a SHP2 inhibitor, with IC50s of 13 nM (Wild-type SHP2), >10000 nM (SHP1), >10000 nM (SHP2 E76K) . SHP2-IN-31 inhibits pERK in a panel of tumor cells. SHP2-IN-31 inhibits tumor growth in RTK/KRAS-driven xenograft models .
SHP2-IN-36 (Compound B8) is an allosteric inhibitor of SHP2, with an IC50 value of 9.0 nM. In addition, its IC50 for p-ERK is 40 nM. SHP2-IN-36 also exhibited significant antitumor activity in the KYSE520 xenograft mouse model. SHP2-IN-36 can be used for research in the field of anti-tumor .
AKT-IN-12 (compound 3e) is a potent Akt kinase inhibitor with an IC50 value of 0.55 μM. AKT-IN-12 induces G0/G1 cell cycle arrest and apoptosis. AKT-IN-12 also inhibits p-AKT, p-ERK, and activates p-JNK, JNK. AKT-IN-12 can be used for researching leukemia .
Anticancer agent 296 is a potent anticancer agent that activates the PERK-eIF2α-CHOP signaling pathway to induce endoplasmic reticulum stress, thereby regulating caspase and Bcl-2 family proteins, ultimately leading to apoptosis. Anticancer agent 296 increases intracellular levels of reactive oxygen species (ROS), reduces mitochondrial membrane potential, and promotes Ca 2+ release. Anticancer agent 296 suppresses cell colony formation and S-phase cell proliferation, and induces autophagy. Anticancer agent 296 is applicable for research on non-small cell lung cancer (NSCLC) .
Peptide R54 acetate (Pep R54 acetate) is a CXCR4 antagonist. Peptide R54 acetate inhibits CXCL12-dependent activation of pERK1/2 and pAKT. The combination of Peptide R54 acetate and Nivolumab (HY-P9903) suppresses melanoma growth. Peptide R54 (acetate) is applicable to research related to melanoma and ovarian cancer .
Cytisine-Platinum(IV) Prodrug-1 is a Pt(IV) prodrug incorporating the natural compound Cytisine (HY-N0175) with antiproliferative activity against tumor cells. Cytisine-Platinum(IV) Prodrug-1 promotes calcium transfer across the IP3R1-GRP75-VDAC1 axis to drive mitochondrial calcium overload. Cytisine-Platinum(IV) Prodrug-1 initiates unfolded protein response via PERK, eIF2α, ATF4, and CHOP to modulate Bcl-2 and Bax, triggering apoptosis. Cytisine-Platinum(IV) Prodrug-1 induces mitochondrial dysfunction, ROS production, reduced ATP synthesis, DNA damage, and S-phase cell cycle arrest. Cytisine-Platinum(IV) Prodrug-1 activates the cGAS-STING pathway, reduces PD-L1 expression, drives immunogenic cell death. Cytisine-Platinum(IV) Prodrug-1 exhibits high physiological stability, efficient cellular accumulation, and enhanced platinum-DNA binding, and inhibits tumor growth in mouse models with reduced systemic toxicity. Cytisine-Platinum(IV) Prodrug-1 can be used for the research of lung cancer .
DPAP is a p-ERK1/2 inhibitor with an IC50 of 7.85 μM against p-ERK1/2. DPAP inhibits the expression of p-MEK1/2 and disrupts the Ras-ERK signaling pathway. DPAP inhibits the expression of COX-2 in nerve cells. DPAP damages DNA and mitochondria, induces Apoptosis via the mitochondrial pathway, and upregulates PD-L1. DPAP inhibits melanoma metastasis and angiogenesis, and inactivates spinal microglia and astrocytes. DPAP exhibits anti-melanoma activity and can be combined with anti-PD-1 monoclonal antibodies to modify anti-tumor effects. DPAP is applicable for the research of melanoma .
KRAS-IN-56 (Compound 18) is a KRAS inhibitor with an EC50 of 33 μM. KRAS-IN-56 inhibits the interaction between GTP-KRAS and SOS1. KRAS-IN-56 induces a decrease in p-ERK levels. KRAS-IN-56 can be used in research related to lung cancer .
NCATS-SM0225 is an endoplasmic reticulum-associated degradation (ERAD) inhibitor and a direct binder of VDAC1, VDAC2 and VDAC3. NCATS-SM0225 exhibits an IC50of 1.02 μM for ERAD and a Kd of 3.13 μM for human VDAC1 binding. NCATS-SM0225 disrupts cellular calcium homeostasis, enhances VDAC1-IP3R coupling and activating PERK. NCATS-SM0225 selectively kills cancer cells, exhibits tumor growth inhibitory effects in melanoma xenograft models. NCATS-SM0225 can be used for research on multiple cancers including melanoma, as well as the molecular mechanisms of ERAD and calcium homeostasis regulation .
ABC294735 is an orally active SK1/SK2 inhibitor. Combination of ABC294735 with Sorafenib (HY-10201) reduces pERK. ABC294735 exhibits anticancer activity against pancreatic adenocarcinoma and renal cell carcinoma. ABC294735 can be used in research related to pancreatic adenocarcinoma and renal cell carcinoma .
ML291 (Standard) is the analytical standard of ML291 (HY-101991). This product is intended for research and analytical applications. ML291 is a UPR (unfolded protein response)-inducing sulfonamidebenzamide. ML291 overwhelms the adaptive capacity of the UPR and induces apoptosis in a variety of solid cancer models. ML291 can activate the PERK/eIF2a/CHOP (apoptotic) arm of the UPR and reduce leukemic cell burden .
Daraxonrasib (RMC-6236) is an orally active, non-covalent RAS (ON) inhibitor. Daraxonrasib disrupts the interaction of wild-type or mutant RAS proteins with the RAS binding domain of BRAF, with EC50 values ranging from 28-220 nM for wild-type KRAS, NRAS, HRAS, and multiple oncogenic RAS variants. Daraxonrasib inhibits pERK. Daraxonrasib has anti-tumor activity against KRAS mutant tumors .
SOS1-IN-25 is an SOS1 inhibitor. SOS1-IN-25 exhibits inhibitory activity against KRAS G12C/SOS1 complex formation (IC50 = 11.11 nM). SOS1-IN-25 leads to a dose-dependent decrease in pERK levels. SOS1-IN-25 can be used for the study of leukemia .
KRAS inhibitor-17 (compound 3-9) is a potent KRAS G12C inhibitor with an IC50 of 3.37 µM. KRAS inhibitor-17 shows p-ERK inhibition activities with IC50s of 9.25, >33.3 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-17 has the potential for the research of pancreatic, colorectal, and lung cancers .
KRAS inhibitor-18 (compound 3-10) is a potent KRAS G12C inhibitor with an IC50 of 4.74 µM. KRAS inhibitor-18 shows p-ERK inhibition activities with IC50s of 66.4, 11.1 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-18 has the potential for the research of pancreatic, colorectal, and lung cancers .
KRAS inhibitor-12 (compound 6-1) is a potent KRAS G12C inhibitor with an IC50 of 0.537 µM. KRAS inhibitor-12 shows p-ERK inhibition activities with IC50s of 1.3, 3.7 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-12 has the potential for the research of pancreatic, colorectal, and lung cancers .
KRAS inhibitor-14 (compound 3-22) is a potent KRAS G12C inhibitor with an IC50 of 0.249 µM. KRAS inhibitor-14 shows p-ERK inhibition activities with IC50s of 1.12, >33.3 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-14 has the potential for the research of pancreatic, colorectal, and lung cancers .
KRAS inhibitor-15 (compound 3-19) is a potent KRAS G12C inhibitor with an IC50 of 0.954 µM. KRAS inhibitor-15 shows p-ERK inhibition activities with IC50s of 2.03, >33.3 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-15 has the potential for the research of pancreatic, colorectal, and lung cancers .
KRAS inhibitor-16 (compound 3-11) is a potent KRAS G12C inhibitor with an IC50 of 0.457 µM. KRAS inhibitor-16 shows p-ERK inhibition activities with IC50s of 3.06, 11.1 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-16 has the potential for the research of pancreatic, colorectal, and lung cancers .
KRAS-IN-54 is a macrocyclic KRAS inhibitor. KRAS-IN-54 exhibits activity against cell viability and pERK inhibition in cells with KRAS G12D and KRAS G13D mutations. KRAS-IN-54 can be used in the research of KRAS-mutant cancers, including pancreatic adenocarcinoma, colorectal cancer, non-small cell lung cancer, esophageal cancer, gallbladder cancer, melanoma, ovarian cancer and endometrial cancer .
CB2 receptor agonist 3 (Standard) is the analytical standard of CB2 receptor agonist 3 (HY-107471). This product is intended for research and analytical applications. CB2 receptor agonist 3 is a robust and selective CB2 cannabinoid agonist with Kis of 7.6 and 900 nM for CB2 and CB1, respectively. CB2 receptor agonist 3 significantly increases P-ERK 1/2 expression in HL-60 cells .
YW3-56 (hydrochloride) is a PAD inhibitor. YW3-56 (hydrochloride) activates p53 target genes. YW3-56 (hydrochloride) activates ATF and blocks autophagy flux. YW3-56 induces ER stress through the PERK-eIF2α-ATF4 signaling cascade and inhibits the mTOR signaling. YW3-56 (hydrochloride) inhibits triple-negative breast cancer .
Vindoline (Standard) is an analytical standard of Vindoline (HY-N0687). This product is intended for research and analytical applications. Vindoline is an orally active vinca alkaloid. Vindoline can be extracted from the leaves of Catharanthus roseus. Vindoline has a weak inhibitory effect on the self-assembly of tubulin. Vindoline alleviates Apoptosis, inhibits p-p65 and p-ERK. Vindoline improves diabetes, bone loss, osteoarthritis, and kidney damage .
Ulixertinib (Standard) is the analytical standard of Ulixertinib. This product is intended for research and analytical applications. Ulixertinib (BVD-523; VRT752271) is a potent, orally active, highly selective, ATP-competitive and reversible covalent inhibitor of ERK1/2 kinases, with an IC50 of <0.3 nM against ERK2. Ulixertinib (BVD-523; VRT752271) inhibits the phosphorylated ERK2 (pERK) and downstream kinase RSK (pRSK) in an A375 melanoma cell line .
KRASG12D-IN-3 is an orally active KRAS G12D inhibitor. KRASG12D-IN-3 inhibits the growth of gastric cancer and pancreatic cancer cells. KRASG12D-IN-3 inhibits the activity of p-ERK in gastric cancer cells. KRASG12D-IN-3 can be used for the research of gastric cancer and pancreatic cancer .
DdBIC is a pyroptosis inducer. DdBIC binds to Nur77 and triggers its translocation to mitochondria, activates SDHA to deplete succinyl-CoA, disrupts heme homeostasis, induces electron leakage, and elicits mitochondrial ROS production. DdBIC induces mitochondrial ROS that oxidatively activates OMA1, promotes OPA1 cleavage and its release into the cytoplasm, activates the integrated stress response via PERK, and ultimately activates granzyme B to cleave GSDMC. DdBIC can be used for the study of melanoma .
Autotaxin-IN-8 (Compound 14E) is an orally active Autotaxin inhibitor with an IC50 of 14.2 nM against hAutotaxin. Autotaxin-IN-8 inhibits Autotaxin activity, MAPK activation, LPAR1 and p-ERK1/2. Autotaxin-IN-8 reduces the phosphorylation levels of JNK and p38. Autotaxin-IN-8 decreases collagen deposition in a mouse model of pulmonary fibrosis. Autotaxin-IN-8 can be used in research related to pulmonary fibrosis .
KRAS-IN-51 (Compound 597a) is a KRas G12V inhibitor, with its IC50 for KRas G12V being 2.9 nM; KD values are 17 (at 20°C) and 68 (at 37°C) nM. KRAS-IN-51 inhibits the phosphorylation of pERK. KRAS-IN-51 has anti-proliferative activity against SW620 and MIAPaCa-2. KRAS-IN-51 can be used for research on colorectal cancer and pancreatic cancer .
PROTAC SOS1 degrader-1 is a potent PROTAC SOS1 degrader with an DC50 of 98.4 nM. PROTAC SOS1 degrader-1 shows antiproliferation activity in cancer cells with various KRAS mutations. PROTAC SOS1 degrader-1 shows antitumor effect with low toxicity .
PROTAC SOS1 degrader-1 (TFA) is a potent PROTAC SOS1 degrader with an DC50 of 98.4 nM. PROTAC SOS1 degrader-1 shows antiproliferation activity in cancer cells with various KRAS mutations. PROTAC SOS1 degrader-1 shows antitumor effect with low toxicity .
KRAS-IN-58 is a KRAS inhibitor with a IC50 of 0.223 μM against KRAS G12D. KRAS-IN-58 binds to KRAS G12C and KRAS G12D proteins, and reduces the levels of phosphorylated Raf1, AKT and ERK in pancreatic cancer cells. KRAS-IN-58 can be used for the research of pancreatic cancer .
Mirdametinib (Standard) is the analytical standard of Mirdametinib (HY-10254). This product is intended for research and analytical applications. Mirdametinib (PD0325901) is an orally active, selective and non-ATP-competitive MEK inhibitor with an IC50 of 0.33 nM. Mirdametinib exhibits a Kiapp of 1 nM against activated MEK1 and MEK2. Mirdametinib suppresses the expression of p-ERK1/2 and induces apoptosis. Mirdametinib has anti-cancer activity for a broad spectrum of human tumor xenografts .
Armepavine, found in Nelumbo nucifera, is an orally active NF-κB inhibitor. Armepavine attenuates expression of p-p65, α-SMA, p-JNK1/2, p-ERK1/2, p-p38α stimulated by TNF-α and LPS. Armepavine suppresses NF-κB nuclear translocation, IκBα phosphorylation, and collagen deposition. Armepavine can be used for the research of hepatic fibrosis and leukemia .
Dosimertinib-d3-d3 is a potent and orally active EGFR inhibitor. Dosimertinib-d3-d3 decreases the expression of p-EGFR and p-ERK protein levels. Dosimertinib-d3-d3 shows antiproliferative and anti-tumor activity. Dosimertinib-d3-d3 has the potential for the research of non-small-cell lung cancer (NSCLC) .
Onalespib (AT13387) is a potent and cross the blood-brain barrier heat-shock-protein-90 (Hsp90) inhibitor. Onalespib inhibits the proliferation, survival and migration. Onalespib decreases the expression of EGFR, p-EGFR, AKT, P-AKT, ERK1/2, P-ERK1/2, S6, P-S6 protein. Onalespib shows antitumor activity. Onalespib has the potential for the research of non-small cell lung cancer (NSCLC) .
KRAS G12C inhibitor 47 (compound 8-1-1) is a potent KRAS G12C inhibitor with an IC50 of 0.172 µM. KRAS G12C inhibitor 47 shows p-ERK inhibition activities with IC50s of 0.046, 69.8 µM in MIA PaCA-2, A549 cells, respectively. KRAS G12C inhibitor 47 has the potential for the research of pancreatic, colorectal, and lung cancers .
EGFR-IN-175 is an orally active and selective EGFR L858R/T790M/C797S inhibitor with an IC50 of 18.94 nM. EGFR-IN-175 can induce cell apoptosis and cause G1 phase arrest. EGFR-IN-175 can downregulate p-EGFR, p-AKT, and p-ERK expression. EGFR-IN-175 can be used for the research of cancer, such as lung cancer .
DGAT-1 inhibitor 2 is an orally active DGAT-1 inhibitor with IC50 values of 15 nM and 9 nM for human DGAT-1 and rat DGAT-1, respectively. DGAT-1 inhibitor 2 increases ROS concentration, GRP78, and PERK protein abundance. DGAT-1 inhibitor 2 increases SREBF1, CPT1A, and MTTP mRNA in fatty acid-treated cells. DGAT-1 inhibitor 2 improves obesity .
Butyrolactone I is an orally active and ATP-competitive inhibitor of CDK1. Butyrolactone I inhibits NF-κB, cdc2 kinase, Bax, ROS production, modulates the PERK/CHOP. Butyrolactone I mitigates heat-stress-induced Apoptosis. Butyrolactone I shows anti-inflammatory and intestinal protective activity. Butyrolactone I has antitumor effects against non-small cell lung, small cell lung, prostate cancer and leukemia. Butyrolactone I can be used in NASH research .
NT-1 (EGFR mutant-IN-3) is a potent mutant EGFR inhibitor and an analog of Osimertinib (HY-15772). This mutant EGFR inhibitor suppresses FGFR WT with an IC50 of 0.4 nM. NT-1 also inhibits EGFR L858R, EGFR Exon 19 deletion and EGFR T790M. NT-1 exerts deeper inhibition on p-EGFR and p-ERK, and induces tumor cell apoptosis. NT-1 can be used in colorectal cancer research .
Setidegrasib (ASP-3082; KRAS G12D inhibitor 17) is a PROTACKRAS degrader (DC50: 37 nM). Setidegrasib induces the degradation of G12D-mutation KRAS protein. Setidegrasib suppresses p-ERK, p-AKT, p-S6 levels in AsPC-1 cells. Setidegrasib exhibits anti-tumor activity in various cancer xenograft models in mice. Setidegrasib can be used for the study of KRAS(G12D)-mutated solid tumors .
KRAS-IN-48 free base (Compound 1-01) is a mutant KRAS inhibitor, with Kd values of 2.58 nM and 5.49 μM for KRAS G12D and KRAS G12V, respectively. KRAS-IN-48 free base affects pERK expression in cells harboring KRAS G12D and KRAS G12V mutations, with IC50 values of 1.1 μM and 1.51 μM, respectively. KRAS-IN-48 free base can be used in the research of cancer .
AG01 is a monoclonal antibody against progranulin (GP88). AG01 inhibits triple-negative breast cancer (TNBC) cell proliferation and migration, reduces the expression of phosphorylated protein kinases p-Src, p-AKT, and p-ERK, and reduces the expression of oncogenic proteins such as Axl, c-MET, HIF-1α, and VEGF. AG01 inhibits tumor growth and Ki67 expression in a TNBC xenograft mouse model. AG01 can be used in the research of TNBC and other cancers .
Ro 67-7476 (Standard) is the analytical standard of Ro 67-7476 (HY-100403). This product is intended for research and analytical applications. Ro 67-7476 is a potent positive allosteric modulator of mGluR1 and potentiates glutamate-induced calcium release in HEK293 cells expressing rat mGluR1a with an EC50 of 60.1 nM . Ro 67-7476 is a potent P-ERK1/2 agonist and activates ERK1/2 phosphorylation in the absence of exogenously added glutamate (EC50=163.3 nM) .
Onalespib lactate is a potent and cross the blood-brain barrier heat-shock-protein-90 (Hsp90) inhibitor with an Kd value of 0.71 nM. Onalespib lactate inhibits the proliferation, survival and migration. Onalespib lactate decreases the expression of EGFR, p-EGFR, AKT, P-AKT, ERK1/2, P-ERK1/2, S6, P-S6 protein. Onalespib lactate shows antitumor activity. Onalespib lactate has the potential for the research of non-small cell lung cancer (NSCLC) .
OSU-2S is a potent PKCδ activator. OSU-2S inhibits cell proliferation and migration. OSU-2S decreases the expression of p-ERK1/2, increases the expression of PKCδ (38 kDa) when combined with Sorafenib (HY-10201). OSU-2S induces Apoptosis. OSU-2S slao is a non-immunosuppressive analogue of FTY720. OSU-2S shows anticancer activity .
GCN2-IN-6 (Compound 6d) is a potent, and orally available GCN2 inhibitor confirmed by in-house enzymatic (IC50 of 1.8 nM) and cellular assays (IC50 of 9.3 nM). GCN2-IN-6 is also a eIF2α kinase PERK inhibitor with an IC50 of 0.26 nM (in enzymatic assay) and 230 nM (in cells) . GCN2-IN-6 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
Tuspetinib (HM43239) is an orally active and selective FLT3 inhibitor with IC50s of 1.1 nM, 1.8 nM and 1.0 nM for FLT3 WT, FLT3 internal tandem duplication (ITD) and FLT3 D835Y kinases, respectively. Tuspetinib inhibits the kinase activity of FLT3 as a reversible type I inhibitor and modulates p-STAT5, p-ERK, SYK, JAK1/2, and TAK1. Tuspetinib inhibits the proliferation and induces the apoptosis of leukemic cells .
Tuspetinib (HM43239) hydrate is an orally active and selective FLT3 inhibitor with IC50s of 1.1 nM, 1.8 nM and 1.0 nM for FLT3 WT, FLT3 internal tandem duplication (ITD) and FLT3 D835Y kinases, respectively. Tuspetinib hydrate inhibits the kinase activity of FLT3 as a reversible type I inhibitor and modulates p-STAT5, p-ERK, SYK, JAK1/2, and TAK1. Tuspetinib hydrate inhibits the proliferation and induces the apoptosis of leukemic cells .
Tuspetinib (HM43239) dihydrochloride is an orally active and selective FLT3 inhibitor with IC50s of 1.1 nM, 1.8 nM and 1.0 nM for FLT3 WT, FLT3 internal tandem duplication (ITD) and FLT3 D835Y kinases, respectively. Tuspetinib dihydrochloride inhibits the kinase activity of FLT3 as a reversible type I inhibitor and modulates p-STAT5, p-ERK, SYK, JAK1/2, and TAK1. Tuspetinib dihydrochloride inhibits the proliferation and induces the apoptosis of leukemic cells .
AZD4625 is an orally active, selective irreversible, covalent allosteric GTPase KRASG12C inhibitor with an IC50 of 3 nM. AZD4625 can inhibit the MAPK pathway (with decreased pCRAF, pMEK, and pERK) and the PI3K pathway (with decreased pAKT and pS6), and induce cell apoptosis. AZD4625 has no binding and inhibition of wild-type RAS or isoforms carrying non-KRASG12C mutations. AZD4625 can be used for the study of KRASG12C mutant non-small cell lung cancer .
Pan-rasin-2 (compound 6A) is an orally active molecular glues that targets RAS. Pan-RAS-IN-2 inhibits pERK (IC50 in AsPC-1 cells: 0.3 nM). Pan-rasin-2 has significant inhibitory activity on cell proliferation of RAS mutant cell lines. Pan-rasin-2 can form ternary complexes with cyclophilin A (CYPA) and RAS (ON) proteins and the formation of ternary complexes can block the binding of RAF downstream of RAS, which has anti-tumor (such as colorectal cancer, pancreatic cancer) effects .
NF-κB/MAPK-IN-2 (compound 14) is a potent NF-κB and MAPK Inhibitor. NF-κB/MAPK-IN-2 decreases the protein expression of p-p65, p-IκB, p-p38, p-JNK, and p-ERK. NF-κB/MAPK-IN-2 reduces the LPS-induced release of TNF-α and IL-6. NF-κB/MAPK-IN-2 inhibits nuclear translocation of p65 and c-Fos. NF-κB/MAPK-IN-2 has the potential for the research of sepsis .
KRAS G12D-IN-36 (Compound 53a) is a highly selective and orally active KRAS-G12D inhibitor with an IC50 of 1.63 nM. KRAS G12D-IN-36 effectively inhibits p-ERK with an IC50 of 8.4 nM. KRAS G12D-IN-36 shows potent anti-proliferative activity against AsPC-1 cells. KRAS G12D-IN-36 can be used for research on pancreatic cancer .
Satratoxin H is a toxic metabolite of Stachybotrys atra. Satratoxin H induces caspase-3 and PARP cleavage via p38 MAPK and JNK pathways, stimulates JNK, ERK, and p38 MAPK phosphorylation, and activates JNK and p38 MAPK in a glutathione-sensitive manner. Satratoxin H induces DNA double-stranded breaks, apoptotic body formation, intracellular reactive oxygen species generation, and endoplasmic reticulum stress via ATF6, PERK, and IRE1 pathways. Satratoxin H can be used for the research of central nervous system disorders and melanoma .
SJF-0628 is a RAF PROTAC degrader. SJF-0628 induces targeted degradation of BRAF in various cancer cell lines (colorectal cancer cell lines (Colo-205, LS-411N, HT-29, RKO) and triple-negative breast cancer cell line DU-4475). SJF-0628 decreases pMEK and pErk levels in DU-4475 cells. SJF-0628 has anti-tumor activity. SJF-0628 can be used for research of colorectal cancer and triple-negative breast cancer .
12-Deoxyphorbol 13-palmitate is a traditional Chinese medicine monomer with antitumor activity that can be isolated from the root of Euphorbia fischeriana. 12-Deoxyphorbol 13-palmitate induces gastric cancer cell cycle arrest and apoptosis by regulating key cell cycle regulators such as cyclin B、cyclin A and CDC2. In addition, 12-Deoxyphorbol 13-palmitate can significantly weaken APOL2–SERCA2–PERK–HES1 signaling and slow liver fibrosis by targeting APOL2 .
VEGFR-2-IN-52 (compound 14d) is a potent VEGFR-2 inhibitor with an IC50 value of 191.1 nM. VEGFR-2-IN-52 decreases the protein expression of p-VEGFR-2, MMP9, p-ERK1/2 and p-MEK1. VEGFR-2-IN-52 shows cytotoxicity. VEGFR-2-IN-52 induces apoptosis and cell cycle arrest at G0/G1 phase. VEGFR-2-IN-52 increases the levels of ROS .
PROTAC FGFR2 degrader 1 (compound N5) is a PROTAC that effectively targets FGFR2 with DC50 of 6.46 nM, the FGFR2IC50 is 0.08 nM. PROTAC FGFR2 degrader 1 has anti-proliferative activity and highly selective, induces G0/G1 arrest of KATOIII and SNU16 cell cycle and inhibits apoptosis by reducing the activation of p-ERK and p-PLCγ, the downstream proteins of FGFR2. PROTAC FGFR2 degrader 1 potently inhibits the growth of SNU16 xenograft tumors in mouse model .
ALK/ROS1-IN-5 (compound X4) is a selective ALK and ROS1 kinases inhibitor with IC50s of 0.512 μM (ALK), 0.766 μM (ROS1), respectively. ALK/ROS1-IN-5 inhibits H2228 cells with an IC50 of 0.034 μM. ALK/ROS1-IN-5 induces cancer cells apoptosis in dose-dependent manner. ALK/ROS1-IN-5 effectively suppresses the expression of p-ALK and p-ERK in cancer cells[1].
Nur77 modulator 4 (Compound 15h) is a Nur77 inducer with a KD of 0.477 μM. Nur77 modulator 4 significantly induces Nur77 expression and apoptosis, showing excellent growth inhibition in HepG2 and MCF-7 cells, with an IC50 of less than 5 μM. Nur77 modulator 4 activates Nur77-mediated ER stress through the PERK-ATF4 and IRE1 signaling pathways, thereby inducing cell apoptosis. Nur77 modulator 4 can be used in cancer research applications .
EGFR-IN-181 is an orally active, potent, brain-penetrant EGFRL858R/T790M/C797S triple mutations inhibitor (IC50 = 1.32 nM). EGFR-IN-181 can inhibit EGFR phosphorylation (p-EGFR) and phosphorylation of its downstream signaling proteins AKT (p-AKT) and ERK (p-ERK). EGFR-IN-181 can induce apoptosis and cause G2 phase arrest. EGFR-IN-181 can be used for the study of non-small cell lung cancer (NSCLC) and brain metastases .
RNK08954 is an orally active KRASG12D inhibitor with a Kd of 0.0395 nM. RNK08954 selectively binds the inactive GDP-bound KRASG12D form, suppresses downstream KRAS-mediated signaling pathways p-ERK1/2 experssion. RNK08954 inhibits KRASG12D-mutant cell proliferation, induces G0-G1 cell cycle arrest, and inhibits tumor growth in mouse xenograft models. RNK08954 can be used for the research of non-small cell lung cancer, pancreatic ductal adenocarcinoma .
NFI23 is a blood-brain barrier-penetrant GluN2B-NMDAR inhibitor, with an IC50 of 1.31 μM and a Ki of 5.98 nM against GluN2B-NMDAR. NFI23 reduces NMDA-induced Ca 2+ influx and ROS production, maintains mitochondrial membrane potential, inhibits neuronal apoptosis, and restores the expression of p-ERK1/2. NFI23 exerts neuroprotective effects against NMDA-induced cytotoxicity and in the rat middle cerebral artery occlusion (MCAO) model. NFI23 can be used for the research of ischemic stroke .
FLT3-IN-31 (compound 10q) is a potent FLT3 inhibitor with IC50 values of 0.16, 2.4 nM for FLT3, FLT3-D835Y, resprctively. FLT3-IN-31 shows antiproliferation activity. FLT3-IN-31 decreases the protein expression of p-FLT3, P-STAT5, P-ERK. FLT3-IN-31 induces apoptosis and cell cycle arrest at G1 phase. FLT3-IN-31 shows antitumor activity .
SOS1-IN-20 (Compound 12f) is an orally active SOS1 inhibitor with an IC50 of 5.11 nM against KRAS G12C::SOS1. By disrupting the interaction between KRAS and SOS1, SOS1-IN-20 inhibits KRAS activation and downstream signal transduction. SOS1-IN-20 has an IC50 of 253 nM for p-ERK in PC-9 cells and 16.71 μM for hERG channel . SOS1-IN-20 can inhibit the proliferation of tumor cells and has antitumor activity .
PROTAC CB1R Degrader-1 is a potent and selective CB1RPROTAC degrader that exploits the ubiquitin-proteasome system (UPS) achieving a DC50 of 3.37 μM in MCF-7 cells and showing no impact on CB2R. PROTAC CB1R Degrader-1 reduces CB1R-associated downstream signaling (p-AKT, p-ERK, BCL2, and MCM5), thereby inhibiting breast cancer cell proliferation and inducing apoptosis. PROTAC CB1R Degrader-1 can be used for breast cancer research .
KRAS G12D-IN-35 (example 7) is a potent and orally active KRAS G12D inhibitor. KRAS G12D-IN-35 suppresses p-ERK in AGS cells and potently inhibits the proliferation of various KRAS G12D-mutant cancer cell lines. KRAS G12D-IN-35 inhibits tumor growth in HPAC and GP2D mouse models. KRAS G12D-IN-35 can be used for cancer research, such as pancreatic and colorectal cancer .
SKLB-D18 is an orally active ERK1/2/ERK5 inhibitor, with an IC50 of 38.69 nM and a Kd of 126.9 nM against human ERK1, an IC50 of 40.12 nM and a Kd of 209.8 nM against ERK2, and an IC50 of 59.72 nM and a Kd of 468.2 nM against ERK5. SKLB-D18 inhibits cancer cell proliferation, induces G0/G1 cell cycle arrest and apoptosis. SKLB-D18 reduces the levels of p-ERK5, p-RSKp90, p-c-Myc and c-Myc, and upregulates the level of p-ERK1/2, thereby inhibiting the ERK1/2/5 pathway in cells. SKLB-D18 increases LC3B-II accumulation, and decreases the levels of p62, p-mTOR and p-p70S6K. SKLB-D18 elevates the levels of ROS, lipid peroxidation and free ferrous ions, reduces the levels of NCOA4 and GPX4, and induces ferritin autophagy-dependent ferroptosis in cancer cells. SKLB-D18 exhibits antitumor activity in a triple-negative breast cancer xenograft mouse model. SKLB-D18 can be used in research related to triple-negative breast cancer .
DGAT-1 inhibitor 2 (Standard) is the analytical standard of DGAT-1 inhibitor 2 (HY-50670). This product is intended for research and analytical applications. DGAT-1 inhibitor 2 is an orally active DGAT-1 inhibitor with IC50 values of 15 nM and 9 nM for human DGAT-1 and rat DGAT-1, respectively. DGAT-1 inhibitor 2 increases ROS concentration, GRP78, and PERK protein abundance. DGAT-1 inhibitor 2 increases SREBF1, CPT1A, and MTTP mRNA in fatty acid-treated cells. DGAT-1 inhibitor 2 improves obesity .
MKK7-JNK activator 1 (Compound 10) is a MKK7-JNK pathway activator. MKK7-JNK activator 1 effectively inhibits the proliferation and migration of MDA-MB-468 cells, induces G2/M phase arrest and caspase -dependent apoptosis (independent of ROS production). MKK7-JNK activator 1 significantly increases the levels of p-MKK7 and p-JNK, but does not affect p-ERK or p-p38. MKK7-JNK activator 1 can be used for the study of triple-negative breast cancer (TNBC) .
TRV055 (TRV120055) is a G protein-biased agonist of angiotensin II type 1 receptors (AT1Rs). TRV120055 induces fibroblast proliferation, overexpression of collagen I and α-SMA, and stress fibre formation in human cardiac fibroblasts. TRV055 activates AT1 receptor/Gαq-mediated signaling pathways, upregulates TGF-β1 and p-ERK1/2. TRV055 induces collagen secretion in adult rat myofibroblasts at a level comparable to Ang II. TRV055 can be used to study the role of G protein-biased signaling of AT1Rs in regulating fibrotic responses [1]
TRV055 (TRV120055) hydrochloride is a G protein-biased agonist of angiotensin II type 1 receptors (AT1Rs). TRV055 hydrochloride induces fibroblast proliferation, overexpression of collagen I and α-SMA, and stress fibre formation in human cardiac fibroblasts. RV055 hydrochloride activates AT1 receptor/Gαq-mediated signaling pathways, upregulates TGF-β1 and p-ERK1/2. RV055 hydrochloride induces collagen secretion in adult rat myofibroblasts at a level comparable to Ang II. RV055 hydrochloride can be used to study the role of G protein-biased signaling of AT1Rs in regulating fibrotic responses [1]
SB-T-101141 is a novel taxane. SB-T-101141 effectively induces a noncanonical ferroptosis to overcome Paclitaxel (HY-B0015) resistance of breast cancer. SB-T-101141 facilitates the production of iron and ferrous ions and ROS. SB-T-101141 stably binds to KHSRP to inhibit the iron-dependent expression of CISD1 related to iron homeostasis. SB-T-101141 synergistically enhances the iron-dependent activation of JNK and PERK pathways via KHSRP. SB-T-101141 suppresses breast tumor growth in MCF-7(PR)/MDA-MB-231(PR) or KHSRP knock-down MCF-7 xenograft mice model .
L-Azetidine-2-carboxylic acid is a proline analog. L-Azetidine-2-carboxylic acid upregulates the lipid autophagy marker LC3-II via activation of the PERK pathway. L-Azetidine-2-carboxylic acid increases pro-apoptotic BAX protein. L-Azetidine-2-carboxylic acid induces ATF6 cleavage and upregulates phosphorylated eIF2α levels. L-Azetidine-2-carboxylic acid induces ER stress, inducing protein misfolding and aggregation. L-Azetidine-2-carboxylic acid shows teratogenic, pro-inflammatory and pro-apoptotic effects .
L-Azetidine-2-carboxylic acid is a proline analog. L-Azetidine-2-carboxylic acid upregulates the lipid autophagy marker LC3-II via activation of the PERK pathway. L-Azetidine-2-carboxylic acid increases pro-apoptotic BAX protein. L-Azetidine-2-carboxylic acid induces ATF6 cleavage and upregulates phosphorylated eIF2α levels. L-Azetidine-2-carboxylic acid induces ER stress, inducing protein misfolding and aggregation. L-Azetidine-2-carboxylic acid shows teratogenic, pro-inflammatory and pro-apoptotic effects .
(3R,10R,14aS)-AZD4625 is the isomer of AZD4625 (HY-146223), and can be used as an experimental control. AZD4625 is an orally active, selective irreversible, covalent allosteric GTPase KRASG12C inhibitor with an IC50 of 3 nM. AZD4625 can inhibit the MAPK pathway (with decreased pCRAF, pMEK, and pERK) and the PI3K pathway (with decreased pAKT and pS6), and induce cell apoptosis. AZD4625 has no binding and inhibition of wild-type RAS or isoforms carrying non-KRASG12C mutations. AZD4625 can be used for the study of KRASG12C mutant non-small cell lung cancer .
BBO-10203 is a potent inhibitor of PI3Kα and KRAS G12C, selectively and covalently binding to Cys242 in the RAS-Binding Domain of PI3Kα, and inhibiting both the GTP-bound and GDP-bound states of KRAS G12C with an IC50 of 0.031 nM and an EC50 of 0.02 nM. BBO-10203 disrupts the interaction between RAS isoforms and PI3Kα, leading to the inhibition of RAS-mediated PI3Kα activation, and reduces pERK expression, cell growth, and induces G1 arrest and apoptosis. BBO-10203 can be used for the research of breast cancer, colorectal cancer, and non-small cell lung cancer .
FLT3-IN-37 (Compound 6z) is a potent inhibitor of FLT3-ITD, with IC50 values of 1.5 and 3.4 nM for FLT3-ITD and TEL-VEGFR2, respectively. FLT3-IN-37 exhibits high selectivity for wild-type FLT3 (WT) and c-Kit. FLT3-IN-37 inhibits FLT3 phosphorylation and downregulates the expression of p-Akt, p-STAT5, and p-ERK. FLT3-IN-37 exerts anti-leukemia effects by blocking the cell cycle and inducing apoptosis (apoptosis). FLT3-IN-37 can be used for research on acute myeloid leukemia (AML) .
FGFR-IN-25 (Compound 19E) is a FGFR inhibitor (IC50s: 1.30 nM and 0.85 nM for FGFR1 and FGFR2, respectively) and radiosensitizer. FGFR-IN-25 effectively reduces the phosphorylation of FGFR1 and its key downstream effectors, pAKT and pERK. FGFR-IN-25 exerts broad-spectrum antitumor activity against gastric cancer, colorectal carcinoma, hepatocellular carcinoma, breast cancer, triple-negative breast cancer, and glioblastoma. FGFR-IN-25, when combined with radiotherapy, synergistically activates the ROS-Caspase-3-GSDME axis, downregulates PD-L1 expression, and induces immunogenic cell death (ICD). FGFR-IN-25 combined with radiotherapy improves the antitumor efficacy .
ISR activator-5 is an eIF2B modulator and integrated stress response (ISR) activator. ISR activator-5 stabilises the inactive I-state of eIF2B, inhibits protein synthesis, and activates canonical ISR pathways without inducing eIF2α phosphorylation. ISR activator-5 can be used for the research of cancer, neurologic and metabolic disorders .
DIM-C-pPhCO2Me is a nuclear receptor 4A1 (NR4A1) antagonist. DIM-C-pPhCO2Me induces Apoptosis. DIM-C-pPhCO2Me decreases PAX3-FOXO1A, N-Myc, Rassf4, MyoD1, Grem1, and DAPK1 proteins. DIM-C-pPhCO2Me decreases expression of TXNDC5 and IDH1, induces markers of ER stress (CHOP, ATF4 and p-PERK). DIM-C-pPhCO2Me inhibits renal cell carcinoma, breast cancer. DIM-C-pPhCO2Me can also be used in rhabdomyosarcoma research .
EGFR T790M/L858R-IN-2 is a potent and selective EGFRT790M/L858R inhibitor with IC50 values of 3.5, 1290 nM for EGFRT790M/L858R, EGFR WT, respectively. EGFR T790M/L858R-IN-2 decreases the expression of p-EGFR, P-AKT, P-ERK1/2. EGFR T790M/L858R-IN-2 induces Apoptosis and cell cycle arrest in the G1 phase. EGFR T790M/L858R-IN-2 shows anti-cancer activity .
MCB-36 is a VHL-recruiting pan-KRAS PROTAC degrader without affecting KRAS transcription. MCB-36 exhibits minimal effects on HRAS and NRAS protein levels. MCB-36 binds to the GDP-loaded state of G12D, G12C, G12V, and wild-type KRAS with high affinities Kd ≈ 1 pM). MCB-36 decreases p-ERK levels, leading to cell apoptosis. MCB-36 effectively suppress KRAS G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-36 can be used for the study of colorectal cancer and lung cancer (Pink: Target protein ligand; Blue: E3 ligand (HY-112078); Black: Linker (HY-W091879)) .
PROTAC DDR1 degrader-1 is a potent and selective DDR1-targeting PROTAC degrader. PROTAC DDR1 degrader-1 selectively induces full-length DDR1 degradation via the ubiquitin proteasome system, blocking downstream signaling pathways. PROTAC DDR1 degrader-1 inhibits tumor cell migration and invasion. PROTAC DDR1 degrader-1 exhibits anti-tumor activity in mice. PROTAC DDR1 degrader-1 can be used for the research of DDR1-driven cancers .
Senkyunolide I is an orally active, blood-brain barrier-permeable metabolite of Z-ligustilide (HY-N0401A) . Senkyunolide I is isolated from Ligusticum chuanxiong. Senkyunolide I upregulates p-Erk1/2 and Nrf2/HO-1, and inhibits Caspase 3. Senkyunolide I alleviates Apoptosis. Senkyunolide I increases the pain threshold in mice and reduces acetic acid-induced writhing responses in mice. Senkyunolide I improves neurological deficits, reduces infarct volume and alleviates cerebral edema in rats with focal cerebral ischemia-reperfusion injury. Senkyunolide I protects renal function and structural integrity in a mouse model of renal ischemia-reperfusion injury. Senkyunolide I is applicable to research related to focal cerebral ischemia-reperfusion injury, migraine, and renal ischemia-reperfusion injury .
Atiprimod (Azaspirane) hydrochloride is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of JAK2 and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of STAT3/NF-κB. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML) .
Atiprimod (Azaspirane) is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of JAK2 and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of STAT3/NF-κB. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML) .
Atiprimod (Azaspirane) (dimaleate) is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of JAK2 and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of STAT3/NF-κB. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML) .
BRAFV600E/ABL2-IN-1 is a BRAFV600E (IC50 = 0.088 μM)/ABL2 (IC50 = 0.3 μM) dual inhibitor. BRAFV600E/ABL2-IN-1 can diminish P-glycoprotein expression. BRAFV600E/ABL2-IN-1 effectively inhibits p-CrkL (Abl2 signaling) and p-ERK1/2 (BRAFV600E pathway) in A375-R melanoma cells. BRAFV600E/ABL2-IN-1 causes cell cycle arrest. BRAFV600E/ABL2-IN-1 significantly increases the percentage of late apoptotic cells. BRAFV600E/ABL2-IN-1 can be used for the study of melanoma .
Bromuconazole is a triazole fungicide with oral efficacy and blood-brain barrier permeability . Bromuconazole protects crops from various fungal contaminations. Bromuconazole exhibits cytotoxicity against a variety of cancer cells, induces G0/G1 cell cycle arrest and inhibits DNA synthesis in cancer cells, and triggers cytoskeletal structural disorder, genotoxic damage, apoptotic (apoptosis) cell death, and mitochondrial membrane depolarization. Bromuconazole activates caspase-3, induces excessive production of ROS, p53 and Bax, lipid peroxidation, increased activities of SOD and CAT, and downregulates Bcl-2. By upregulating p-ERK1/2 and p-JNK, Bromuconazole disrupts the MAPK signaling pathway, impairs the cellular stress response of human trophoblast cells and endometrial cells, and damages the implantation process . Bromuconazole is applicable to research related to glioma, colon cancer, reproductive injury (implantation dysfunction), and cardiac dysfunction .
Molibresib besylate (GSK 525762C; I-BET 762 besylate) is an orally active pan-BET inhibitor that targets and binds to BRD2, BRD3, BRD4 and BRDT. By competitively occupying acetylated lysine binding sites, Molibresib besylate disrupts the interaction between BET proteins and chromatin, thereby effectively inhibiting MYC expression and target gene transcription. Molibresib besylate exhibits broad antiproliferative activity, which not only inhibits cancer cell growth and induces growth arrest, but also downregulates mitosis-related genes and upregulates the level of p-ERK1/2. When combined with MEK inhibitors, Molibresib besylate shows a significant synergistic effect, reduces tumor burden in mouse models of leukemia, modulates the immune microenvironment and prolongs survival. Molibresib besylate is widely applicable to research related to acute myeloid leukemia, multiple myeloma, triple-negative breast cancer, small-cell lung cancer and various advanced refractory solid tumors .
STX-721 is an orally active, irreversible, covalent EGFR exon 20 insertion (ex20ins) inhibitor that selectively targets ex20ins-mutant dynamic protein states. STX-721 potently inhibits the kinase activity of EGFR ex20ins mutants (NPG, ASV, SVD). STX-721 inhibits phosphorylation of EGFR (pEGFR Y1068) and downstream ERK (pERK Thr202/Tyr204), and suppresses proliferation of ex20ins-mutant Ba/F3 cells and human NSCLC cell lines (NCI-H2073 ASV KI, CUTO-14 ASV). STX-721 induces tumor regression in EGFR ex20ins-mutant PDX/CDX models. STX-721 can be used for the study of non-small cell lung cancer (NSCLC) harboring EGFR or HER2 ex20ins mutations .
MAPK-IN-3 (Compound 4a) is an anti-proliferative agent that shows particularly strong inhibitory effects on KYSE 30, HCT 116, and HGC 27, with IC50 values of 0.57 μM, 3.27 μM, and 2.28 μM, respectively. MAPK-IN-3 blocks the cell cycle via a p53-dependent mechanism and induces cell apoptosis through a p53-independent mechanism. MAPK-IN-3 downregulates the expression of cell cycle-related proteins like Cyclin D1 and cyclin B1, upregulates pro-apoptotic proteins such as cleaved PARP, cleaved caspase-7, and cleaved caspase-9, and reduces the expression of anti-apoptotic proteins like Bcl-2. Additionally, MAPK-IN-3 increases the intracellular level of ROS in KYSE 30 cells and upregulates the expression of members of the MAPK signaling pathway associated with ROS, such as p-ERK, p-p38 and p-JNK .
EGFR/tubulin-IN-1 (Compound 26) is a dual-target inhibitor of EGFR and tubulin. EGFR/tubulin-IN-1 significantly reduces the levels of p-EGFR, p-AKT, and p-ERK in cells, disrupting the microtubule structure of the cells. EGFR/tubulin-IN-1 significantly inhibits the proliferation of H1975 cells and significantly blocks the cells in the G2/M phase. EGFR/tubulin-IN-1 induces the expression of autophagy markers LC3B-II and Beclin-1, while down-regulating the expression of p62. EGFR/tubulin-IN-1 induces ferroptosis, with increased ROS content and depletion of glutathione (GSH). EGFR/tubulin-IN-1 inhibits epithelial-mesenchymal transition (EMT) and tumor metastasis. EGFR/tubulin-IN-1 has a significant tumor-suppressing effect in the H1975 transplanted tumor nude mouse model. EGFR/tubulin-IN-1 can be used for the study of non-small cell lung cancer .
Murine Thrombin is a murine serine protease that plays a central role in blood coagulation. Murine Thrombin stimulates macrophages to polarize into a unique phenotype characterized by anti-inflammatory and pro-repair properties. Murine Thrombin activates PAR1, induces the production of MCP-1, MMP3 and VEGF in mouse intervertebral discs, and causes degradation of the cartilage matrix and destruction of intervertebral disc structure. Murine Thrombin activity increases significantly in paraoxon-induced status epilepticus .
6-Methoxyflavone (Standard) is the analytical standard of 6-Methoxyflavone (HY-W097625). This product is intended for research and analytical applications. 6-Methoxyflavone is an orally active methoxyflavone. 6-Methoxyflavone suppresses neuroinflammation in microglia through the inhibition of TLR4/MyD88/p38 MAPK/NF-κB dependent pathways and the activation of HO-1/NQO-1 signaling. 6-Methoxyflavone induces S-phase arrest through the CCNA2/CDK2/p21CIP1 signaling pathway and activates the PERK/EIF2a/ATF4/CHOP pathway in HeLa cells. 6-Methoxyflavone acts as a Flumazenil (HY-B0009)-insensitive positive allosteric modulator at human recombinant α1β2γ2L and α2β2γ2L GABAα receptors. 6-Methoxyflavone inhibits NFAT Translocation into the nucleus and suppresses T cell activation. 6-Methoxyflavone partially restores chronic ethanol-induced behavioral deficits in mice. 6-Methoxyflavone antagonizes chronic constriction injury and diabetes associated neuropathic nociception expression. 6-Methoxyflavone can be used for the study of cancer, inflammation and neurological diseases .
Endoplasmic reticulum (ER) contributes to the production and folding of approximately one third of cellular proteins, and is thus inextricably linked to the maintenance of cellular homeostasis and the fine balance between health and disease. However, some adverse factors negatively impact ER functions and protein synthesis, resulting in the activation of Endoplasmic reticulum stress (ER stress, ERS) and unfolded protein response (UPR) signaling pathways. The UPR is triggered when ER protein folding capacity is overwhelmed by cellular demand and the UPR initially aims to restore ER homeostasis and normal cellular functions. However, if this fails, then the UPR triggers cell death. Chronic ER stress and defects in UPR signaling are emerging as key contributors to a growing list of human diseases, including diabetes, neurodegeneration and cancer.
MCE Endoplasmic Reticulum Stress Compound Library contains 363 ER stress-related compounds that mainly target PERK, IRE1, ATF6, etc. MCE ER stress library is a useful tool for researching ER stress and related diseases.
TRV055 (TRV120055) is a G protein-biased agonist of angiotensin II type 1 receptors (AT1Rs). TRV120055 induces fibroblast proliferation, overexpression of collagen I and α-SMA, and stress fibre formation in human cardiac fibroblasts. TRV055 activates AT1 receptor/Gαq-mediated signaling pathways, upregulates TGF-β1 and p-ERK1/2. TRV055 induces collagen secretion in adult rat myofibroblasts at a level comparable to Ang II. TRV055 can be used to study the role of G protein-biased signaling of AT1Rs in regulating fibrotic responses [1]
TRV055 (TRV120055) hydrochloride is a G protein-biased agonist of angiotensin II type 1 receptors (AT1Rs). TRV055 hydrochloride induces fibroblast proliferation, overexpression of collagen I and α-SMA, and stress fibre formation in human cardiac fibroblasts. RV055 hydrochloride activates AT1 receptor/Gαq-mediated signaling pathways, upregulates TGF-β1 and p-ERK1/2. RV055 hydrochloride induces collagen secretion in adult rat myofibroblasts at a level comparable to Ang II. RV055 hydrochloride can be used to study the role of G protein-biased signaling of AT1Rs in regulating fibrotic responses [1]
FGF7p is a small molecule peptide and a potential bladder protector. FGF7p can activate downstream signaling pathways of FGFR2 in the urinary tract epithelium (pFRS2α, pAKT and pERK). FGF7p alleviates cyclophosphamide induced apoptosis and tissue damage in urinary tract epithelial cells by activating AKT and its downstream anti apoptotic targets (pBAD, pS6/mTORC1). FGF7p is commonly used in the study of inflammatory conditions .
Teverelix (EP 24332) is a GnRH antagonist. Teverelix binds competitively and reversibly to GnRH receptors, thereby suppressing the release of LH and FSH. Teverelix can be used in the research of prostatic hyperplasia, endometriosis, and prostate cancer .
Peptide R54 acetate (Pep R54 acetate) is a CXCR4 antagonist. Peptide R54 acetate inhibits CXCL12-dependent activation of pERK1/2 and pAKT. The combination of Peptide R54 acetate and Nivolumab (HY-P9903) suppresses melanoma growth. Peptide R54 (acetate) is applicable to research related to melanoma and ovarian cancer .
AG01 is a monoclonal antibody against progranulin (GP88). AG01 inhibits triple-negative breast cancer (TNBC) cell proliferation and migration, reduces the expression of phosphorylated protein kinases p-Src, p-AKT, and p-ERK, and reduces the expression of oncogenic proteins such as Axl, c-MET, HIF-1α, and VEGF. AG01 inhibits tumor growth and Ki67 expression in a TNBC xenograft mouse model. AG01 can be used in the research of TNBC and other cancers .
L-Azetidine-2-carboxylic acid is a proline analog. L-Azetidine-2-carboxylic acid upregulates the lipid autophagy marker LC3-II via activation of the PERK pathway. L-Azetidine-2-carboxylic acid increases pro-apoptotic BAX protein. L-Azetidine-2-carboxylic acid induces ATF6 cleavage and upregulates phosphorylated eIF2α levels. L-Azetidine-2-carboxylic acid induces ER stress, inducing protein misfolding and aggregation. L-Azetidine-2-carboxylic acid shows teratogenic, pro-inflammatory and pro-apoptotic effects .
Bufotalin is a steroid lactone isolated from Venenum Bufonis with potently antitumor activities. Bufotalin induces cancer cell apoptosis and also induces endoplasmic reticulum (ER) stress activation .
Senkyunolide I is an orally active, blood-brain barrier-permeable metabolite of Z-ligustilide (HY-N0401A) . Senkyunolide I is isolated from Ligusticum chuanxiong. Senkyunolide I upregulates p-Erk1/2 and Nrf2/HO-1, and inhibits Caspase 3. Senkyunolide I alleviates Apoptosis. Senkyunolide I increases the pain threshold in mice and reduces acetic acid-induced writhing responses in mice. Senkyunolide I improves neurological deficits, reduces infarct volume and alleviates cerebral edema in rats with focal cerebral ischemia-reperfusion injury. Senkyunolide I protects renal function and structural integrity in a mouse model of renal ischemia-reperfusion injury. Senkyunolide I is applicable to research related to focal cerebral ischemia-reperfusion injury, migraine, and renal ischemia-reperfusion injury .
Sulforaphene, isolated from radish seeds, exhibits an ED50 against velvetleaf seedlings approximately 2 x 10 -4 M. Sulforaphene promotes cancer cells apoptosis and inhibits migration via inhibiting EGFR, p-ERK1/2, NF‐κB and other signals .
1,2,4-Trihydroxybenzene (Hydroxyhydroquinone) is an ER stress inducer that targets proteins such as PKR-like ER kinase PERK to induce cytotoxicity. 1,2,4-Trihydroxybenzene selectively activates eIF2α phosphorylation, activates the PERK-eIF2α signaling pathway and induces stress granule formation. 1,2,4-Trihydroxybenzene subsequently exacerbates oxidative stress and causes DNA double-strand breaks, destroying organelles such as mitochondria and ER, and inducing cell death. 1,2,4-Trihydroxybenzene also has the potential to exhibit anti-tumor effect, increase blood pressure, and relieve spasm .
Vindoline is an orally active vinca alkaloid. Vindoline can be extracted from the leaves of Catharanthus roseus. Vindoline has a weak inhibitory effect on the self-assembly of tubulin. Vindoline alleviates Apoptosis, inhibits p-p65 and p-ERK. Vindoline improves diabetes, bone loss, osteoarthritis, and kidney damage .
Armepavine, found in Nelumbo nucifera, is an orally active NF-κB inhibitor. Armepavine attenuates expression of p-p65, α-SMA, p-JNK1/2, p-ERK1/2, p-p38α stimulated by TNF-α and LPS. Armepavine suppresses NF-κB nuclear translocation, IκBα phosphorylation, and collagen deposition. Armepavine can be used for the research of hepatic fibrosis and leukemia .
Isogosferol ((+)-Isogospherol; Isogospherol) is a potent anti-inflammatory agent. Isogosferol decreases LPS (HY-D1056)-stimulated NO and IL-1β expression. Isogosferol decreases the LPS (HY-D1056)-stimulated expression of iNOS, COX-2, NF-κB, and pERK1/2 .
Sulforaphene, isolated from radish seeds, exhibits an ED50 against velvetleaf seedlings approximately 2 x 10-4 M. Sulforaphene promotes cancer cells apoptosis and inhibits migration via inhibiting EGFR, p-ERK1/2, NF‐κB and other signals .
Vindoline (Standard) is an analytical standard of Vindoline (HY-N0687). This product is intended for research and analytical applications. Vindoline is an orally active vinca alkaloid. Vindoline can be extracted from the leaves of Catharanthus roseus. Vindoline has a weak inhibitory effect on the self-assembly of tubulin. Vindoline alleviates Apoptosis, inhibits p-p65 and p-ERK. Vindoline improves diabetes, bone loss, osteoarthritis, and kidney damage .
L-Azetidine-2-carboxylic acid is a proline analog. L-Azetidine-2-carboxylic acid upregulates the lipid autophagy marker LC3-II via activation of the PERK pathway. L-Azetidine-2-carboxylic acid increases pro-apoptotic BAX protein. L-Azetidine-2-carboxylic acid induces ATF6 cleavage and upregulates phosphorylated eIF2α levels. L-Azetidine-2-carboxylic acid induces ER stress, inducing protein misfolding and aggregation. L-Azetidine-2-carboxylic acid shows teratogenic, pro-inflammatory and pro-apoptotic effects .
Bufotalin is a steroid lactone isolated from Venenum Bufonis with potently antitumor activities. Bufotalin induces cancer cell apoptosis and also induces endoplasmic reticulum (ER) stress activation .
1,2,4-Trihydroxybenzene (Hydroxyhydroquinone) (Standard) is the analytical standard of 1,2,4-Trihydroxybenzene (HY-W010451). This product is intended for research and analytical applications. 1,2,4-Trihydroxybenzene (Hydroxyhydroquinone) is an ER stress inducer that targets proteins such as PKR-like ER kinase PERK to induce cytotoxicity. 1,2,4-Trihydroxybenzene selectively activates eIF2α phosphorylation, activates the PERK-eIF2α signaling pathway and induces stress granule formation. 1,2,4-Trihydroxybenzene subsequently exacerbates oxidative stress and causes DNA double-strand breaks, destroying organelles such as mitochondria and ER, and inducing cell death. 1,2,4-Trihydroxybenzene also has the potential to exhibit anti-tumor effect, increase blood pressure, and relieve spasm .
Satratoxin H is a toxic metabolite of Stachybotrys atra. Satratoxin H induces caspase-3 and PARP cleavage via p38 MAPK and JNK pathways, stimulates JNK, ERK, and p38 MAPK phosphorylation, and activates JNK and p38 MAPK in a glutathione-sensitive manner. Satratoxin H induces DNA double-stranded breaks, apoptotic body formation, intracellular reactive oxygen species generation, and endoplasmic reticulum stress via ATF6, PERK, and IRE1 pathways. Satratoxin H can be used for the research of central nervous system disorders and melanoma .
12-Deoxyphorbol 13-palmitate is a traditional Chinese medicine monomer with antitumor activity that can be isolated from the root of Euphorbia fischeriana. 12-Deoxyphorbol 13-palmitate induces gastric cancer cell cycle arrest and apoptosis by regulating key cell cycle regulators such as cyclin B、cyclin A and CDC2. In addition, 12-Deoxyphorbol 13-palmitate can significantly weaken APOL2–SERCA2–PERK–HES1 signaling and slow liver fibrosis by targeting APOL2 .
6-Methoxyflavone (Standard) is the analytical standard of 6-Methoxyflavone (HY-W097625). This product is intended for research and analytical applications. 6-Methoxyflavone is an orally active methoxyflavone. 6-Methoxyflavone suppresses neuroinflammation in microglia through the inhibition of TLR4/MyD88/p38 MAPK/NF-κB dependent pathways and the activation of HO-1/NQO-1 signaling. 6-Methoxyflavone induces S-phase arrest through the CCNA2/CDK2/p21CIP1 signaling pathway and activates the PERK/EIF2a/ATF4/CHOP pathway in HeLa cells. 6-Methoxyflavone acts as a Flumazenil (HY-B0009)-insensitive positive allosteric modulator at human recombinant α1β2γ2L and α2β2γ2L GABAα receptors. 6-Methoxyflavone inhibits NFAT Translocation into the nucleus and suppresses T cell activation. 6-Methoxyflavone partially restores chronic ethanol-induced behavioral deficits in mice. 6-Methoxyflavone antagonizes chronic constriction injury and diabetes associated neuropathic nociception expression. 6-Methoxyflavone can be used for the study of cancer, inflammation and neurological diseases .
Dosimertinib-d5 (mesylate) is a potent and orally active EGFR inhibitor. Dosimertinib-d5 (mesylate) decreases the expression of p-EGFR and p-ERK protein levels. Dosimertinib-d5 (mesylate) shows antiproliferative and anti-tumor activity. Dosimertinib-d5 (mesylate) has the potential for the research of non-small-cell lung cancer (NSCLC) .
Dosimertinib-d3-d3 is a potent and orally active EGFR inhibitor. Dosimertinib-d3-d3 decreases the expression of p-EGFR and p-ERK protein levels. Dosimertinib-d3-d3 shows antiproliferative and anti-tumor activity. Dosimertinib-d3-d3 has the potential for the research of non-small-cell lung cancer (NSCLC) .
Milnacipran-d10 (hydrochloride) is the deuterium labeled Milnacipran hydrochloride (HY-B0168A). Milnacipran hydrochloride is an orally active Serotonin (HY-B1473A) and Norepinephrine (HY-13715) reuptake inhibitor. Milnacipran hydrochloride inhibits monoamine transporters, especially the norepinephrine transporter and the serotonin transporter (Ki values of 31 and 8.5 nM, respectively). Milnacipran hydrochloride inhibits pERK1/2 activation. Milnacipran hydrochloride has antidepressant, anxiolytic and analgesic properties. Milnacipran hydrochloride inhibits biting behavior in mice. Milnacipran hydrochloride can be used in the study of major depressive disorder, anxiety disorders, and neuropathic pain (e.g., fibromyalgia) .
PERK-IN-4-d3 is the deuterium labeled PERK-IN-4. PERK-IN-4 is a potent and selective PERK (protein kinase R (PKR)-like endoplasmic reticulum kinase) inhibitor with an IC50 of 0.3 nM. PERK is activated in response to a variety of endoplasmic reticulum stresses implicated in numerous disease states .
Milnacipran-d5 hydrochloride is deuterium labeled Milnacipran hydrochloride (HY-B0168A). Milnacipran hydrochloride is an orally active Serotonin (HY-B1473A) and Norepinephrine (HY-13715) reuptake inhibitor. Milnacipran hydrochloride inhibits monoamine transporters, especially the norepinephrine transporter and the serotonin transporter (Ki values of 31 and 8.5 nM, respectively). Milnacipran hydrochloride inhibits pERK1/2 activation. Milnacipran hydrochloride has antidepressant, anxiolytic and analgesic properties. Milnacipran hydrochloride inhibits biting behavior in mice. Milnacipran hydrochloride can be used in the study of major depressive disorder, anxiety disorders, and neuropathic pain (e.g., fibromyalgia) .
KRAS G12D-IN-35 (example 7) is a potent and orally active KRAS G12D inhibitor. KRAS G12D-IN-35 suppresses p-ERK in AGS cells and potently inhibits the proliferation of various KRAS G12D-mutant cancer cell lines. KRAS G12D-IN-35 inhibits tumor growth in HPAC and GP2D mouse models. KRAS G12D-IN-35 can be used for cancer research, such as pancreatic and colorectal cancer .
MCB-36 is a VHL-recruiting pan-KRAS PROTAC degrader without affecting KRAS transcription. MCB-36 exhibits minimal effects on HRAS and NRAS protein levels. MCB-36 binds to the GDP-loaded state of G12D, G12C, G12V, and wild-type KRAS with high affinities Kd ≈ 1 pM). MCB-36 decreases p-ERK levels, leading to cell apoptosis. MCB-36 effectively suppress KRAS G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-36 can be used for the study of colorectal cancer and lung cancer (Pink: Target protein ligand; Blue: E3 ligand (HY-112078); Black: Linker (HY-W091879)) .
KRAS-IN-48 free base (Compound 1-01) is a mutant KRAS inhibitor, with Kd values of 2.58 nM and 5.49 μM for KRAS G12D and KRAS G12V, respectively. KRAS-IN-48 free base affects pERK expression in cells harboring KRAS G12D and KRAS G12V mutations, with IC50 values of 1.1 μM and 1.51 μM, respectively. KRAS-IN-48 free base can be used in the research of cancer .
KRAS G12D-IN-36 (Compound 53a) is a highly selective and orally active KRAS-G12D inhibitor with an IC50 of 1.63 nM. KRAS G12D-IN-36 effectively inhibits p-ERK with an IC50 of 8.4 nM. KRAS G12D-IN-36 shows potent anti-proliferative activity against AsPC-1 cells. KRAS G12D-IN-36 can be used for research on pancreatic cancer .
RNK08954 is an orally active KRASG12D inhibitor with a Kd of 0.0395 nM. RNK08954 selectively binds the inactive GDP-bound KRASG12D form, suppresses downstream KRAS-mediated signaling pathways p-ERK1/2 experssion. RNK08954 inhibits KRASG12D-mutant cell proliferation, induces G0-G1 cell cycle arrest, and inhibits tumor growth in mouse xenograft models. RNK08954 can be used for the research of non-small cell lung cancer, pancreatic ductal adenocarcinoma .
Eif2ak3 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Eif2ak3 gene (Mouse), as well as a negative control, a positive control, and a FAM-labeled negative control.
EIF2AK3 Human Pre-designed siRNA Set A contains three designed siRNAs for EIF2AK3 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
Lamp1 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Lamp1 gene (Mouse), as well as a negative control, a positive control, and a FAM-labeled negative control.
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Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
MedchemExpress Validation 03
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
MedchemExpress Validation 04
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
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