Search Result

Results for "

pERK/pAKT

" in MedChemExpress (MCE) Product Catalog:

By Targets:	PERK (7) Akt (14) Apoptosis (10) Atg8/LC3 (1) Autophagy (1) Bcl-2 Family (1) c-Met/HGFR (1) Cannabinoid Receptor (1) Caspase (1) CXCR (1) EGFR (5) ERK (9) Ferroptosis (1) FGFR (2) FLT3 (1) HIF/HIF Prolyl-Hydroxylase (1) HSP (2) JNK (1) Lipase (1) MEK (2) Microtubule/Tubulin (1) MMP (1) mTOR (1) p38 MAPK (3) p62 (1) PD-1/PD-L1 (1) PI3K (5) PROTACs (2) Pyroptosis (1) Raf (1) Ras (5) Reactive Oxygen Species (ROS) (2) SHP2 (2) Src (1) STAT (1) TAM Receptor (1) VEGFR (2)
By Research Areas:	Cancer (22) Inflammation/Immunology (1) Metabolic Disease (1) Neurological Disease (2)

By Targets:

PERK (7)

Akt (14)

Apoptosis (10)

Atg8/LC3 (1)

Autophagy (1)

Bcl-2 Family (1)

c-Met/HGFR (1)

Cannabinoid Receptor (1)

Caspase (1)

CXCR (1)

EGFR (5)

ERK (9)

Ferroptosis (1)

FGFR (2)

FLT3 (1)

HIF/HIF Prolyl-Hydroxylase (1)

HSP (2)

JNK (1)

Lipase (1)

MEK (2)

Microtubule/Tubulin (1)

MMP (1)

mTOR (1)

p38 MAPK (3)

p62 (1)

PD-1/PD-L1 (1)

PI3K (5)

PROTACs (2)

Pyroptosis (1)

Raf (1)

Ras (5)

Reactive Oxygen Species (ROS) (2)

SHP2 (2)

Src (1)

STAT (1)

TAM Receptor (1)

VEGFR (2)

By Research Areas:

Cancer (22)

Inflammation/Immunology (1)

Metabolic Disease (1)

Neurological Disease (2)

Inhibitors & Agonists

Peptides

Inhibitory Antibodies

Natural
Products

Targets Recommended: PERK

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-148273

Setidegrasib ASP-3082; KRAS G12D inhibitor 17	PROTACs Ras ERK Akt	Cancer
Setidegrasib (KRAS G12D inhibitor 17, ASP3082) is a PROTAC KRAS 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. (Blue: VHL ligase ligand (HY-168699); Black: linker (HY-168698); Pink: G12D ligand (HY-168700)) .

HY-14463

Onalespib Maximum Cited Publications 11 Publications Verification AT13387	HSP	Cancer
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) .

HY-N0777

Isorhamnetin-3-O-glucoside 3 Publications Verification	Others PERK ERK Akt PI3K Lipase	Metabolic Disease
Isorhamnetin-3-O-glucoside is an orally active natural compound. Isorhamnetin 3-O-glucoside increases *P-ERK, ERK, P-Akt* (Ser473), P-PI3K, and PDX-1. Isorhamnetin 3-O-glucoside downregulates C/EBPα and inhibits lipase. Isorhamnetin 3-O-glucoside reduces lipids and inhibits obesity .

HY-153663

TH-Z827	Ras	Cancer
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 .

HY-P11162

FGF7p	FGFR Akt ERK mTOR Apoptosis	Inflammation/Immunology
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 .

HY-P991664

AG01	Src Akt ERK TAM Receptor c-Met/HGFR MMP HIF/HIF Prolyl-Hydroxylase VEGFR	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 .

HY-113916

Onalespib lactate AT13387 lactate	HSP	Cancer
Onalespib lactate is a potent and cross the blood-brain barrier heat-shock-protein-90 (Hsp90) inhibitor with an K_d 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) .

HY-146223

AZD4625	Ras p38 MAPK PI3K Apoptosis	Cancer
AZD4625 is an orally active, selective irreversible, covalent allosteric GTPase KRAS^G12C 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-KRAS^G12C mutations. AZD4625 can be used for the study of KRAS^G12C mutant non-small cell lung cancer .

HY-178176

PROTAC CB1R Degrader-1	PROTACs Cannabinoid Receptor Akt ERK Bcl-2 Family Apoptosis	Cancer
PROTAC CB1R Degrader-1 is a potent and selective CB1R PROTAC 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. (Blue: CRBN ligand (HY-41547); Black: linker (HY-178198); Pink: CB1R ligand (HY-134497)) .

HY-178939

EGFR-IN-181	EGFR Akt PERK Apoptosis	Neurological Disease Cancer
EGFR-IN-181 is an orally active, potent, brain-penetrant EGFR^{L858R/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 .

HY-146223A

(3R,10R,14aS)-AZD4625	Ras PI3K p38 MAPK Apoptosis	Cancer
(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 KRAS^G12C 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-KRAS^G12C mutations. AZD4625 can be used for the study of KRAS^G12C mutant non-small cell lung cancer .

HY-155098

CNBCA	SHP2	Cancer
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 .

HY-173188

EGFR-IN-154	EGFR Akt PERK JNK p38 MAPK	Cancer
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 .

HY-173573

TK-684	Apoptosis SHP2	Cancer
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 .

HY-144693

MEK/PI3K-IN-2	MEK PI3K PERK	Cancer
MEK/PI3K-IN-2 (compound 6s) is a potent MEK/PI3K inhibitor, with IC₅₀ values of 352 nM (MEK1), 107 nM (PI3Kα), and 137 nM (PI3Kδ), respectively. MEK/PI3K-IN-2 suppresses pAKT and pERK1/2 levels. MEK/PI3K-IN-2 shows anti-proliferative activity against tumor cell lines .

HY-144692

MEK/PI3K-IN-1	MEK PI3K PERK	Cancer
MEK/PI3K-IN-1 (compound 6r) is a potent MEK/PI3K inhibitor, with IC₅₀ values of 124 nM (MEK1), 130 nM (PI3Kα), and 236 nM (PI3Kδ), respectively. MEK/PI3K-IN-1 suppresses pAKT and pERK1/2 levels. MEK/PI3K-IN-1 shows anti-proliferative activity against tumor cell lines .

HY-147513

AKT-IN-12	Akt Apoptosis	Cancer
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 .

HY-178009

EGFR-IN-175	EGFR Apoptosis Akt PERK	Cancer
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 .

HY-149824

EGFR T790M/L858R-IN-2	EGFR Apoptosis	Cancer
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 .

HY-179049

EGFR/tubulin-IN-1	EGFR Microtubule/Tubulin Akt ERK Autophagy Atg8/LC3 p62 Ferroptosis Reactive Oxygen Species (ROS)	Cancer
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 .

HY-P11011A

Peptide R54 acetate Pep R54 acetate; CXCR4 antagonist peptide 19 acetate	CXCR ERK Akt	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 .

HY-182749

KRAS-IN-58	Ras Akt Raf ERK	Cancer
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 .

HY-179497

FLT3-IN-37	FLT3 VEGFR Akt STAT ERK Apoptosis	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) .

HY-181005

FGFR-IN-25	FGFR Akt PERK Reactive Oxygen Species (ROS) Caspase Pyroptosis PD-1/PD-L1	Neurological Disease Cancer
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 .

Cat. No.	Product Name	Target	Research Area