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Pathways Recommended: MAPK/ERK Pathway
Results for "

pERK pathway

" in MedChemExpress (MCE) Product Catalog:

29

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1

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3

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6

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-W050044
    L-Azetidine-2-carboxylic acid
    1 Publications Verification

    		 Endogenous Metabolite PERK Atg8/LC3 Autophagy Bcl-2 Family Apoptosis Eukaryotic Initiation Factor (eIF) ATF6 Cardiovascular Disease Neurological Disease Metabolic Disease Endocrinology Cancer
    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
  • HY-114164G
    Murine Thrombin

    		Thrombin Protease Activated Receptor (PAR) MMP VEGFR Epigenetic Reader Domain Cardiovascular Disease Neurological Disease Inflammation/Immunology
    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 .
    Murine Thrombin
  • HY-W010451
    1,2,4-Trihydroxybenzene

    Hydroxyhydroquinone

    		 PERK Eukaryotic Initiation Factor (eIF) Potassium Channel Apoptosis Cardiovascular Disease Cancer
    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 .
    1,2,4-Trihydroxybenzene
  • HY-P3136
    TRV055

    TRV120055

    		 Angiotensin Receptor ERK Cardiovascular Disease
    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
  • HY-158196
    PERK/eIF2α activator 1

    		PERK Apoptosis Cancer
    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 .
    PERK/eIF2α activator 1
  • HY-P3136A
    TRV055 hydrochloride

    TRV120055 hydrochloride

    		 Angiotensin Receptor Cardiovascular Disease
    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]
    TRV055 hydrochloride
  • 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 .
    FGF7p
  • HY-13559
    Atiprimod

    Azaspirane ; SKF 106615-12; SKF 106615A12

    		 STAT Apoptosis Autophagy Reactive Oxygen Species (ROS) Caspase Bcl-2 Family p62 Atg8/LC3 PARP NF-κB PERK JAK Cardiovascular Disease Inflammation/Immunology Cancer
    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
  • HY-146223
    AZD4625

    		Ras p38 MAPK PI3K Apoptosis Cancer
    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 .
    AZD4625
  • HY-173119
    SKLB-D18

    		ERK Autophagy Apoptosis p62 mTOR Reactive Oxygen Species (ROS) Ferroptosis 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 .
    SKLB-D18
  • HY-121033
    BS148

    		Sigma Receptor p38 MAPK Apoptosis Cancer
    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 .
    BS148
  • 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 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 .
    (3R,10R,14aS)-AZD4625
  • HY-13559A
    Atiprimod dimaleate

    Azaspirane dimaleate; SKF 106615-12 dimaleate; SKF 106615A12 dimaleate

    		 STAT Apoptosis Caspase Interleukin Related Autophagy Reactive Oxygen Species (ROS) Atg8/LC3 p62 JAK Cardiovascular Disease Inflammation/Immunology Cancer
    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) .
    Atiprimod dimaleate
  • HY-110102
    Atiprimod hydrochloride

    Azaspirane hydrochloride; SKF 106615-12 hydrochloride; SKF 106615

    		 JAK STAT Apoptosis Autophagy Reactive Oxygen Species (ROS) Caspase Atg8/LC3 p62 Cardiovascular Disease Inflammation/Immunology Cancer
    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 hydrochloride
  • HY-W050044R
    L-Azetidine-2-carboxylic acid (Standard)

    		Reference Standards Endogenous Metabolite PERK Atg8/LC3 Autophagy Bcl-2 Family Apoptosis Eukaryotic Initiation Factor (eIF) ATF6 Cardiovascular Disease Neurological Disease Metabolic Disease Endocrinology Cancer
    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 (Standard)
  • HY-106159
    SB-T-101141

    		Reactive Oxygen Species (ROS) p38 MAPK JNK PERK Ferroptosis Cancer
    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 .
    SB-T-101141
  • HY-123647
    Satratoxin H

    		Endogenous Metabolite p38 MAPK JNK Caspase PARP ERK Apoptosis Reactive Oxygen Species (ROS) Infection 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 .
    Satratoxin H
  • HY-149918
    Antiproliferative agent-23

    		Microtubule/Tubulin Apoptosis Cancer
    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 .
    Antiproliferative agent-23
  • HY-W010451R
    1,2,4-Trihydroxybenzene (Standard)

    Hydroxyhydroquinone (Standard)

    		 Reference Standards PERK Potassium Channel Apoptosis Eukaryotic Initiation Factor (eIF) Cardiovascular Disease Cancer
    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 .
    1,2,4-Trihydroxybenzene (Standard)
  • HY-170849
    Nur77 modulator 4

    		Nuclear Hormone Receptor 4A/NR4A Apoptosis PERK IRE1 Cancer
    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 .
    Nur77 modulator 4
  • HY-179044
    MKK7-JNK activator 1

    		p38 MAPK JNK Caspase Apoptosis Cancer
    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) .
    MKK7-JNK activator 1
  • HY-178382
    BRAFV600E/ABL2-IN-1

    		Raf Bcr-Abl P-glycoprotein PERK Apoptosis Cancer
    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 .
    BRAFV600E/ABL2-IN-1
  • HY-169412
    MAPK-IN-3

    		MDM-2/p53 CDK Caspase Bcl-2 Family Reactive Oxygen Species (ROS) p38 MAPK ERK JNK Cancer
    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 .
    MAPK-IN-3
  • HY-181087
    Anticancer agent 296

    		PERK Apoptosis Autophagy Reactive Oxygen Species (ROS) Caspase Bcl-2 Family Cancer
    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) .
    Anticancer agent 296
  • HY-182360
    Cytisine-platinum(IV) prodrug-1

    		PERK Eukaryotic Initiation Factor (eIF) Bcl-2 Family Apoptosis Reactive Oxygen Species (ROS) STING DNA/RNA Synthesis PD-1/PD-L1 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 .
    Cytisine-platinum(IV) prodrug-1
  • HY-182899
    DPAP

    		PERK Ras COX PD-1/PD-L1 Apoptosis DNA/RNA Synthesis Mitochondrial Metabolism 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 .
    DPAP
  • HY-180200
    RNK08954

    		Ras ERK 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 .
    RNK08954
  • HY-W097625R
    6-Methoxyflavone (Standard)

    		Toll-like Receptor (TLR) MyD88 p38 MAPK NF-κB Heme Oxygenase (HO) Reference Standards PERK Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    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 .
    6-Methoxyflavone (Standard)
  • HY-W715812
    Bromuconazole

    		Fungal Apoptosis Caspase Reactive Oxygen Species (ROS) MDM-2/p53 SOD Bcl-2 Family PERK JNK p38 MAPK Cardiovascular Disease Infection Endocrinology Cancer
    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 .
    Bromuconazole

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