654 Results for "

caspase activation

" in MedChemExpress (MCE) Product Catalog:
Products (654)

654 Results for "caspase activation" in MCE Product Catalog:

Cat. No.: HY-153939S
Purity:  99.57%
Synonyms: RG7388-d3-1
Idasanutlin-d3-1 (RG7388-d3-1) is the deuterated-labeled Idasanutlin (HY-15676). Idasanutlin (RG7388) is an orally bioavailable MDM2 inhibitor with an IC50 of 6 nM. Idasanutlin disrupts MDM2-p53 binding, stabilizes and activates p53, triggering cell cycle arrest, apoptosis, and reduced cancer cell viability. Idasanutlin reduces EGFR protein expression and phosphorylation, suppresses downstream SHP2, MEK1/2, ERK1/2, AKT, mTOR, p70(S6K1), and S6 signaling. Idasanutlin induces mitochondrial ROS production, drives p38 MAPK phosphorylation, upregulates NOXA, and mediates caspase-3-dependent apoptosis and gasdermin E-mediated pyroptosis. Idasanutlin can be used for the research of TP53-mutant non-small cell lung cancer, T-cell acute lymphoblastic leukemia, colorectal carcinoma, melanoma, diffuse large B-cell lymphoma, mantle cell lymphoma, non-Hodgkin lymphoma, severe fever with thrombocytopenia syndrome, neuroblastoma, acute lymphoblastic leukemia, relapsed or refractory acute myeloid leukemia, osteosarcoma, solid tumors, and hematological tumors .
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Cat. No.: HY-15676R
CAS No.: 1229705-06-9
Synonyms: RG7388 (Standard)
Idasanutlin (Standard) (RG7388 (Standard)) is the analytical standard of Idasanutlin (HY-15676). This product is intended for research and analytical applications. Idasanutlin (RG7388) is an orally bioavailable MDM2 inhibitor with an IC50 of 6 nM. Idasanutlin disrupts MDM2-p53 binding, stabilizes and activates p53, triggering cell cycle arrest, apoptosis, and reduced cancer cell viability. Idasanutlin reduces EGFR protein expression and phosphorylation, suppresses downstream SHP2, MEK1/2, ERK1/2, AKT, mTOR, p70(S6K1), and S6 signaling. Idasanutlin induces mitochondrial ROS production, drives p38 MAPK phosphorylation, upregulates NOXA, and mediates caspase-3-dependent apoptosis and gasdermin E-mediated pyroptosis. Idasanutlin can be used for the research of TP53-mutant non-small cell lung cancer, T-cell acute lymphoblastic leukemia, colorectal carcinoma, melanoma, diffuse large B-cell lymphoma, mantle cell lymphoma, non-Hodgkin lymphoma, severe fever with thrombocytopenia syndrome, neuroblastoma, acute lymphoblastic leukemia, relapsed or refractory acute myeloid leukemia, osteosarcoma, solid tumors, and hematological tumors .
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Cat. No.: HY-120281
CAS No.: 2126038-25-1
Target:  

MEK PI3K Akt Apoptosis Caspase

Research Areas:  

Cancer

ST-168 is an orally active MEK/PI3K inhibitor with an IC50 of 182 nM against MEK1 and IC50 values ​​of 69.2, 41.7, 1482 and 2293 nM against PI3Kα, PI3Kδ, PI3Kβ and PI3Kγ respectively. ST-168 completely inhibits the phosphorylation of ERK1/2 and AKT and induces cancer cell death in a 3D tumor sphere model. ST-168 demonstrates significant antitumor effects in the A375 melanoma mouse model. ST-168 improves the ocular toxicity profile of MEK inhibitors, showing lower caspase activation levels, indicating reduced apoptosis induction. ST-168 can be used in melanoma research .
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Cat. No.: HY-P2040
CAS No.: 118399-22-7
Nodularin is a hepatotoxin, tumor promoter, and protein phosphatase inhibitor. Nodularin induces apoptosis (apoptosis) in normal cells (including caspase activation, upregulation of Bcl-XS, and upregulation of BAX/P53), triggers hyperphosphorylation of the MAPK/ERK, mTOR/S6K and p38 MAPK signaling pathways, and induces oxidative stress, endoplasmic reticulum membrane instability, peroxisome proliferation and increased lysosomal enzyme activity. Nodularin promotes DEN (HY-N7434)-initiated hepatocyte proliferation and adenoma formation, and inhibits proliferation, phagocytosis and chemotaxis of normal lymphocytes, oocyte maturation and vitellogenesis, as well as angiogenesis. Nodularin exhibits hepatotoxicity, reproductive and endocrine toxicity, and embryonic developmental toxicity in various animal models. Nodularin can be used in studies related to liver cancer, hepatotoxicity and reproductive endocrine toxicity .
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Cat. No.: HY-P10414
Synonyms: KP1 (human)
Target:  

TGF-β Receptor

Research Areas:  

Infection Endocrinology

Klotho-derived peptide 1 (KP1 (human)) is a polypeptide with multiple activities including senescence inhibition and renal protection. Klotho-derived peptide 1 binds to TβR2 and ATAD3A, with a Kd value of 1.41 μM for binding to human TβR2 and a Kd value of 0.319 μM for binding to ATAD3A. By binding to TβR2, Klotho-derived peptide 1 blocks the TGF-β/Smad3 and downstream TGF-β signaling pathways, inhibits the expression of miR-223-3p, induces the expression of lncRNA-TUG1, restores endogenous Klotho at the post-transcriptional level, inhibits cellular senescence markers, fibroblast activation and renal tubular epithelial cell apoptosis, blocks cytochrome c release and caspase activation, maintains the integrity of mitochondrial ultrastructure, and restores mitochondrial protein levels. Klotho-derived peptide 1 enters renal tubular epithelial cells via endocytosis, protects against nephrotoxic and hypoxic injuries, and recapitulates the renal protective and anti-fibrotic effects of full-length Klotho. Klotho-derived peptide 1 can be used in research related to kidney diseases such as chronic kidney disease and SARS-CoV-2-associated acute kidney injury .
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Cat. No.: HY-P10414A
Synonyms: KP1 (human) hydrochloride
Target:  

TGF-β Receptor

Research Areas:  

Infection Endocrinology

Klotho-derived peptide 1 hydrochloride (KP1 (human) hydrochloride) is a polypeptide with multiple activities including senescence inhibition and renal protection. Klotho-derived peptide 1 hydrochloride binds to TβR2 and ATAD3A, with a Kd value of 1.41 μM for binding to human TβR2 and a Kd value of 0.319 μM for binding to ATAD3A. By binding to TβR2, Klotho-derived peptide 1 hydrochloride blocks the TGF-β/Smad3 and downstream TGF-β signaling pathways, inhibits the expression of miR-223-3p, induces the expression of lncRNA-TUG1, restores endogenous Klotho at the post-transcriptional level, inhibits cellular senescence markers, fibroblast activation and renal tubular epithelial cell apoptosis, blocks cytochrome c release and caspase activation, maintains the integrity of mitochondrial ultrastructure, and restores mitochondrial protein levels. Klotho-derived peptide 1 hydrochloride enters renal tubular epithelial cells via endocytosis, protects against nephrotoxic and hypoxic injuries, and recapitulates the renal protective and anti-fibrotic effects of full-length Klotho. Klotho-derived peptide 1 hydrochloride can be used in research related to kidney diseases such as chronic kidney disease and SARS-CoV-2-associated acute kidney injury .
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Cat. No.: HY-187534
Research Areas:  

Cancer

VEGFR2 AUTOTAC-1 is a VEGFR2 AUTOTAC degrader. VEGFR2 AUTOTAC-1 recruits p62, activates the autophagy-lysosome pathway through the p62-LC3 axis cascade, forms a ternary complex with VEGFR2 and p62, and drives UPS-independent post-translational degradation of VEGFR2. VEGFR2 AUTOTAC-1 induces G1 phase arrest and endogenous apoptosis in cells via the mitochondrial and caspase apoptotic pathways, thereby inhibiting cancer cell proliferation, migration and malignant phenotypes; meanwhile, it inhibits endothelial cell tube formation, migration and endothelial-mesenchymal transition by regulating E-cadherin and MMP2. VEGFR2 AUTOTAC-1 is applicable to research related to triple-negative breast cancer.(Pink: VEGFR2 target protein ligand (HY-187558); Blue: p62 ligand (HY-W014292); Black: Linker)
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Cat. No.: HY-P992072

Target:  

Apoptosis Caspase

Research Areas:  

Metabolic Disease

Anti-Human/Mouse CD95 Antibody (HFE7A) is an antibody targeting human/mouse Fas (CD95), with a Kd of 1.6 nM in mice. Anti-Human/Mouse CD95 Antibody (HFE7A) modulates the Fas-mediated apoptotic signaling pathway without blocking the binding of Jo2 to Fas. Anti-Human/Mouse CD95 Antibody (HFE7A) inhibits Jo2-induced caspase activation, mitochondrial depolarization, hepatocyte death and apoptosis. Anti-Human/Mouse CD95 Antibody (HFE7A) protects BALB/c mice against Jo2-induced acute liver injury and reduces Jo2-associated elevation of serum transaminase levels. Anti-Human/Mouse CD95 Antibody (HFE7A) can be used in studies related to liver injury. For isotype control, refer to Mouse IgG1 kappa, Isotype Control (HY-P99977) .
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Cat. No.: HY-N17617
CAS No.: 70238-51-6
S-Petasin is a phosphodiesterase (PDE) inhibitor with IC50 values of 25.5 μM and 17.5 μM for PDE3 and PDE4, respectively. S-Petasin inhibits cholesterol side-chain cleavage enzyme, 11β-hydroxylase, PPAR-γ, and iNOS induction at RNA and protein levels. S-Petasin induces apoptosis, activates caspases, cleaves PARP, modulates mitochondrial membrane permeability, and regulates BCL2/BAX, p53, Bcl-XL, MMP-2, MMP-9, p21, CDK4, and cyclin D1 expression. S-Petasin reduces inflammatory cell accumulation, cytokine and IgE levels, and enhances serum IgG2a levels. S-Petasin relaxes isolated sensitized guinea pig trachealis and exhibits gastrointestinal anti-spasmodic activity. S-Petasin reduces tonsillitis severity and asthmatic attack frequency. S-Petasin can be used for the research of prostate cancer, obesity, melanoma, allergic asthma, asthma, and peritonitis .
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Cat. No.: HY-P5763
CAS No.: 1415039-77-8
Synonyms: PNX-20
Phoenixin-20 (PNX-20) is a neuropeptide that activates GPR173. Phoenixin-20 inhibits LPS-induced TLR-4/MyD88/NF-κB signaling, pro-inflammatory cytokines, adhesion molecules, MMPs, and cytotoxicity. Phoenixin-20 increases SIRT1 and inhibits NLRP3/ASC/caspase-1, oxidative stress, and IL-1β/IL-18. Phoenixin-20 alleviates ox-LDL-induced endothelial dysfunction, monocyte adhesion, adhesion molecules, cytokines, NADPH oxidase/NOX-4, and ROS. Phoenixin-20 promotes GPR173/STAT6-mediated anti-inflammatory polarization of microglia and neuroprotection. Phoenixin-20 can be used in research on dental pulp infection, pulmonary arterial hypertension, atherosclerosis, neuroinflammation, anxiety, and neurodegenerative diseases .
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Cat. No.: HY-117087
CAS No.: 1071544-43-8
Target:  

Phosphatase PANoptosis

Research Areas:  

Cancer

K103 is an inhibitor discovered from the screen that is an analog of the serotonin antagonist benzazocine. K103 exhibited inhibition of SHIP homologues, labelling it a pan-SHIP1/2 inhibitor, but the molecule had no effect on another 5' inositol phosphatase, OCRL. In line with the "two PIPs hypothesis", the molecule exhibited significant anti-tumour effects against a variety of cell lines, particularly breast cancer cells. Additional studies with K103 revealed that inhibition of SHIP1/2 in multiple myeloma cells resulted in G2/M cell cycle arrest followed by extensive apoptosis via activation of the caspase cascade. K103 fits the commonly used small molecule agent property profile, but while this work was being conducted, it was discovered that K103 caused psychoactive effects in mice, which limited the utility of the molecule in vivo. Therefore, certain synthetic studies were conducted on this tryptamine to identify the features that needed to be present in the molecule to maintain pan-SHIP1/2 inhibition in order to design an inhibitor with favourable pharmacodynamic properties and an improved side effect profile.
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Cat. No.: HY-N0559R
CAS No.: 52659-56-0
Kirenol (Standard) is the analytical standard of Kirenol (HY-N0559). This product is intended for research and analytical applications. Kirenol is a diterpenoid compound, an orally active apoptosis inducer and signaling pathway regulator, with a Kd value of 5.47 μM against the target CK2. Kirenol promotes the cleavage of Bid into tBid, regulates the protein levels/phosphorylation of Bax, Bcl-2, p53 and p21, and induces caspase-independent apoptosis, S-phase cell cycle arrest, ROS accumulation and cytotoxicity in cancer cells. Kirenol activates the CK2/AKT and AMPK-mTOR-ULK1 pathways, inhibits the signaling of NF-κB, TGF-β/Smads and NLRP3 inflammasome, and regulates the GSK3β, BMP and Wnt/β-catenin pathways. Kirenol induces autophagy, mitophagy and osteoblast differentiation, promotes mitochondrial fusion, and exerts antioxidant, anti-inflammatory, antifibrotic, renoprotective, cardioprotective, neuroprotective and analgesic effects. Kirenol is applicable to research related to chronic myeloid leukemia, ischemic stroke, diabetic nephropathy, heart failure, acute lung injury and osteoporosis.
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Cat. No.: HY-P5763A
Synonyms: PNX-20 TFA
Phoenixin-20 TFA (PNX-20 TFA) is a neuropeptide that activates GPR173. Phoenixin-20 TFA inhibits LPS-induced TLR-4/MyD88/NF-κB signaling, pro-inflammatory cytokines, adhesion molecules, MMPs, and cytotoxicity. Phoenixin-20 TFA increases SIRT1 and inhibits NLRP3/ASC/caspase-1, oxidative stress, and IL-1β/IL-18. Phoenixin-20 TFA alleviates ox-LDL-induced endothelial dysfunction, monocyte adhesion, adhesion molecules, cytokines, NADPH oxidase/NOX-4, and ROS. Phoenixin-20 TFA promotes GPR173/STAT6-mediated anti-inflammatory polarization of microglia and neuroprotection. Phoenixin-20 TFA can be used in research on dental pulp infection, pulmonary arterial hypertension, atherosclerosis, neuroinflammation, anxiety, and neurodegenerative diseases .
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Cat. No.: HY-184501
CAS No.: 486440-74-8
Research Areas:  

Cancer

UE01 is an orally active, selective small-molecule modulator targeting both ULK1/ERK1/2. UE01 activates hULK1 with an EC50 of 695.30 nM and a KD of 114.3 nM for ULK1; it inhibits hERK1 with an IC50 of 179.90 nM and a KD of 114 nM for ERK1; it shows weak binding to ERK2 with a KD of 2.8 mM. UE01 induces the conformational transition of ULK1 from an inactive to an active state, enhances the phosphorylation of ULK1 Ser317 and mAtg13 Ser355, and reduces the phosphorylation of ULK1 Ser757. UE01 competitively occupies the ATP-binding pocket of ERK1, inhibits ERK1 kinase activity, and reduces the activity of the ERK1/2 signaling pathway. UE01 induces complete autophagy flux and apoptosis, upregulates Atg5, Atg7, LC3-II/LC3-I, Bax, cytochrome C (Cyt c), Cleaved-Caspase 3, Cleaved-PARP1 and E-cadherin, downregulates p62, Bcl-2, MMP-2 and MMP-9, reduces the phosphorylation of Exo70 Ser250, and promotes the proteasome-dependent degradation of Cav-1, thereby inhibiting EMT-related phenotypes and extracellular matrix degradation. UE01 can be used in studies related to triple-negative breast cancer .
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