2. Signaling Pathways
  3. Apoptosis
  4. Caspase

Caspase

Caspase

Related Products

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Caspase is a family of cysteine proteases that play essential roles in apoptosis (programmed cell death), necrosis, and inflammation. There are two types of apoptotic caspases: initiator (apical) caspases and effector (executioner) caspases. Initiator caspases (e.g., CASP2, CASP8, CASP9, and CASP10) cleave inactive pro-forms of effector caspases, thereby activating them. Effector caspases (e.g., CASP3, CASP6, CASP7) in turn cleave other protein substrates within the cell, to trigger the apoptotic process. The initiation of this cascade reaction is regulated by caspase inhibitors. CASP4 and CASP5, which are overexpressed in some cases of vitiligo and associated autoimmune diseases caused by NALP1 variants, are not currently classified as initiator or effector in MeSH, because they are inflammatory enzymes that, in concert with CASP1, are involved in T-cell maturation.

Caspase Isoform Specific Products:

Caspase Isoform Comparison
Cat. No. Product Name Effect Purity Chemical Structure
  • HY-P10452
    Ac-LEVDGWK(Dnp)-NH2
    Ac-LEVDGWK(Dnp)-NH2 is a substrate for Caspase-3, and can be used to detect Caspase-3 activity.
    Ac-LEVDGWK(Dnp)-NH2
  • HY-P4401A
    Z-VEID-AFC TFA
    Z-VEID-AFC TFA is the trifluoroacetate salt of Z-VEID-AFC (HY-P4401). Z-VEID-AFC TFA is a fluorescent substrate for caspase-6. When Z-VEID-AFC TFA is cleaved by caspase-6, 7-amino-4-trifluoromethylcoumarin (AFC) is released, and its fluorescence can be used to quantify caspase-6 activity (Ex/Em: 400/505 nm) .
    Z-VEID-AFC TFA
  • HY-182937
    FLC-8
    		Activator
    FLC-8 is an orally active FLT3 inhibitor with IC50 values of 10.2 nM, 11.6 nM and 24.10 nM against human FLT3-WT, FLT3-G697R and FLT3-N676D, respectively. FLC-8 inhibits FLT3 autophosphorylation and downstream STAT5, AKT and ERK signaling pathways, and induces apoptosis in acute myeloid leukemia (AML) cells. FLC-8 exhibits potent antitumor activity in the MV4-11 xenograft model. FLC-8 can be used for the research of acute myeloid leukemia.
    FLC-8
  • HY-182759
    MN33-47
    		Activator
    MN33-47 is a multi-target anti-tumor compound with broad-spectrum anti-proliferative activity. MN33-47 relieves the inhibition of the mitochondrial apoptosis pathway by downregulating the anti-apoptotic protein Bcl-2, while activating caspase-3 and inhibiting Topoisomerase I activity, thereby promoting its degradation through the ubiquitin-proteasome and autophagy-lysosome pathways. MN33-47 can also induce DNA cross-linking and G2/M cell cycle arrest, inhibit cancer cell migration and activate the mitochondrial apoptosis pathway, thus exerting potent anti-tumor effects. MN33-47 can improve the water solubility of SN-38 (HY-13704), and exhibits dose-dependent tumor growth inhibition effects in CT26 tumor-bearing mouse models without obvious toxic and side effects. MN33-47 can be used in related studies on colorectal adenocarcinoma, cervical adenocarcinoma, hepatocellular carcinoma, alveolar basal epithelial adenocarcinoma, gastric cancer and colon cancer.
    MN33-47
  • HY-P10832
    ATWLPPRAANLLMAAS
    		Activator
    ATWLPPRAANLLMAAS is a chimeric peptide with anti-angiogenic and potent anti-tumor effects. ATWLPPRAANLLMAAS can inhibit the proliferation, viability, migration, and invasion of human hepatocellular carcinoma cells, and induce apoptosis..
    ATWLPPRAANLLMAAS
  • HY-182391
    MKI-3
    		Modulator
    MKI-3 is a selective microtubule-associated serine/threonine kinase-like (MASTL) inhibitor with an IC50 of 5.72 nM and a Kd of 1.89 nM. MKI-3 disrupts the MASTL-ENSA-Aurora A signaling axis. MKI-3 induces chromosomal instability, mitotic catastrophe and apoptosis (apoptosis) in cancer cells. MKI-3 is applicable to research related to triple-negative breast cancer.
    MKI-3
  • HY-P4392
    Z-VAD-AMC
    Z-VAD-AMC is a substrate of caspase-9.
    Z-VAD-AMC
  • HY-N16733
    Deacetyltanghinin
    		Activator
    Deacetyltanghinin is a selective inhibitor targeting Na+/K+ ATPase, acting through non-covalent binding but is highly cardiotoxic. Deacetyltanghinin inhibits Na+/K+ ATPase activity, induces cancer cell apoptosis (involving caspase pathway activation), and at the same time affect the TXA2-PGI2 balance in the rabbit heart. Deacetyltanghinin has significant anti-cancer activity and is mainly used in the research field of targeted therapy of malignant tumors such as breast cancer and lung cancer. At the same time, attention should be paid to the regulation of its cardiotoxicity.
    Deacetyltanghinin
  • HY-132974
    Aminoflavone
    		Activator
    Aminoflavone is an anti-tumor agent. Aminoflavone inhibits the expression of ITGA6/SOX2 by activating the AhR-miR-125b-2-3p axis, thereby targeting breast cancer stem cells. Aminoflavone induces an increase in intracellular ROS, increases the level of oxidative DNA damage marker 8-oxodG and DNA-protein cross-links. Aminoflavone causes S-phase arrest, activates caspase-3/8/9 and induces apoptosis (apoptosis). Aminoflavone inhibits HIF-1α expression in a manner independent of AhR. Aminoflavone can be used for the study of breast cancer.
    Aminoflavone
  • HY-P10241
    Ac-LEHD-CHO
    		Inhibitor
    Ac-LEHD-CHO is an inhibitor for caspase 8/9. Ac-LEHD-CHO prevents GalN/TNF-α-induced hepatotoxicity and hepatocyte apoptosis.
    Ac-LEHD-CHO
  • HY-19696S2
    Tauroursodeoxycholate-d4-1
    		Inhibitor
    Tauroursodeoxycholate-d4-1 is the deuterium labeled Tauroursodeoxycholate. Tauroursodeoxycholate (Tauroursodeoxycholic acid) is an endoplasmic reticulum (ER) stress inhibitor. Tauroursodeoxycholate significantly reduces expression of apoptosis molecules, such as caspase-3 and caspase-12. Tauroursodeoxycholate also inhibits ERK.
    Tauroursodeoxycholate-d<sub>4</sub>-1
  • HY-182008
    NEURL1B-IN-1
    		Modulator
    NEURL1B-IN-1 is a molecular glue-like NEURL1B degrader with a Kd value of 46.2 nM. NEURL1B-IN-1 binds to Arg422 within the NHR2 domain of NEURL1B, triggers its autoubiquitination and proteasomal degradation, disrupts its interaction with DLL1, and attenuates the Notch signaling pathway. NEURL1B-IN-1 induces cell cycle arrest and apoptosis, and inhibits migration of hepatocellular carcinoma cells. NEURL1B-IN-1 is applicable to research related to hepatocellular carcinoma.
    NEURL1B-IN-1
  • HY-P1094
    AZ-10417808
    		Inhibitor
    AZ-10417808 is a selective caspase-3 inhibitor. AZ-10417808 blocks apoptosis signaling pathway by inhibiting caspase-3 activity. AZ-10417808 can be used to study the effect of nicotine on plasmacytoid dendritic cell migration.
    AZ-10417808
  • HY-N16771
    Clausenidin
    		Activator
    Clausenidin is a selective inhibitor targeting apoptosis-related pathways, including the mitochondrial pathway and death receptor pathway, and vascular endothelial growth factor (VEGF). Clausenidin induces mitochondrial membrane depolarization by activating caspase-3, caspase-8 and caspase-9, upregulating the pro-apoptotic protein Bax and downregulating the anti-apoptotic protein Bcl-2. Clausenidin also inhibits VEGF expression and blocks angiogenesis, exerting anti-tumor activity. Clausenidin has inhibitory effects against Mycobacterium tuberculosis (MIC=200 μg/mL). Clausenidin can induce apoptosis in liver cancer cells, arrest the cell cycle in the G2/M phase, and inhibit tumor angiogenesis. Clausenidin can be used in the research of malignant tumors such as liver cancer.
    Clausenidin
  • HY-178133
    Pim-1 kinase-IN-14
    		Activator
    Pim-1 kinase-IN-14 is a PIM-1 kinase inhibitor with an IC50 value of 94 nM. Pim-1 kinase-IN-14 shows broad-spectrum and high-efficiency anticancer activity against multiple human cancer cell lines, including liver cancer (HepG-2), colon cancer (Caco-2), myeloid leukemia (NFS-60), and prostate cancer (PC-3) cells. Pim-1 kinase-IN-14exerts its anticancer effects by inducing apoptosis and activating caspase 3/7. Pim-1 kinase-IN-14 can be used for the study of cancers associated with PIM-1 kinase overexpression.
    Pim-1 kinase-IN-14
  • HY-W714898
    2-Hexadecanol
    		Activator 98.0%
    2-Hexadecanol is a fatty acid based compound. 2-Hexadecanol can be isolated from marine organism Sea pen. 2-Hexadecanol induces Apoptosis, elevates the expression of caspase-3 and caspase-8. 2-Hexadecanol exhibits anticancer activity against breast cancer and cervical cancer.
    2-Hexadecanol
  • HY-126956
    Porphyra 334
    		Inhibitor
    Porphyra 334 is a carnosine-like amino acid and a natural photoprotective agent and antioxidant. Porphyra-334 exerts its photoprotective effects by scavenging ROS, inhibiting the expression and activity of MMP-1/8, and promoting the synthesis of collagen and elastin. Porphyra 334 effectively inhibits linoleic acid oxidation induced by alkyl radicals (AAPH) and singlet oxygen. Porphyra 334 has anti-obesity potential by inhibiting the expression of PPARγ2 and C/EBPα. Porphyra 334 protects cells against UV-induced DNA damage and apoptosis by inhibiting the activation of caspase-3.
    Porphyra 334
  • HY-180941
    Bfl-1-IN-7
    		Activator
    Bfl-1-IN-7 (Compound 25) is a selective, covalent, orally active Bfl-1 inhibitor with an IC50 of 0.015 μM. Bfl-1-IN-7 elicits Caspase activation. Bfl-1-IN-7 can be used in cancer research.
    Bfl-1-IN-7
  • HY-178380
    HDAC8-IN-14
    		Activator
    HDAC8-IN-14, a curcuminoid derivative, is a selective HDAC8 inhibitor with a Ki of 9 nM. HDAC8-IN-14 induces the production of reactive oxygen species (ROS), disrupts mitochondrial membrane potential, and promotes apoptosis. HDAC8-IN-14 can significantly promote the accumulation of cells in the sub-G0/G1 phase, consistent with apoptotic or necrotic cell death. HDAC8-IN-14 induces upregulation of cytochrome c, cleaved caspase-3, and the pro-apoptotic protein Bak while leaving the anti-apoptotic Bcl-2 levels unaltered. HDAC8-IN-14 can be used for the study of leukemia.
    HDAC8-IN-14
  • HY-N19463
    Dicatenarin
    		Activator
    Dicatenarin is a caspase‑3 activator with growth‑inhibitory activity against human cancer cells. Dicatenarin increases caspase‑3 activity, induces intracellular ROS generation, and activates the mitochondrial‑mediated apoptotic pathway. Dicatenarin exerts growth‑inhibitory effects against a panel of human cancer cell lines. Dicatenarin can be used in research on pancreatic cancer, lung cancer, colon cancer, breast cancer, prostate cancer, and ovarian cancer.
    Dicatenarin
Cat. No. Product Name / Synonyms Species Source
Cat. No. Product Name / Synonyms Application Reactivity
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Download Caspase Signaling Pathway Map.

Upon binding to their cognate ligand, death receptors such as Fas and TRAILR can activate initiator Caspases (Pro-caspase 8 and Pro-caspase 10) through dimerization mediated by adaptor proteins such as FADD and TRADD. Active Caspase 8 and Caspase 10 then cleave and activate the effector Caspase 3, 6 and 7, leading to apoptosis. ROS/DNA damage and ER stress trigger Caspase 2 activation. Active Caspase 2 cleaves and activates Caspase 3 and initiates apoptosis directly. Caspase 2, 8 and 10 can also cleave Bid, stimulate mitochondrial outer membrane permeabilization (MOMP) and initiate the intrinsic apoptotic pathway. Following MOMP, mitochondrial intermembrane space proteins such as Smac and Cytochrome C are released into the cytosol. Cytochrome C interacts with Apaf-1, triggering apoptosome assembly, which activates Caspase 9. Active Caspase 9, in turn, activates Caspase 3, 6 and 7, leading to apoptosis. Mitochondrial release of Smac facilitates apoptosis by blocking the inhibitor of apoptosis (IAP) proteins. 

 

Following the binding of TNF to TNFR1, TNFR1 binds to TRADD, which recruits RIPK1, TRAF2/5 and cIAP1/2 to form TNFR1 signaling complex I. Formation of the complex IIa and complex IIb is initiated either by RIPK1 deubiquitylation mediated by CYLD or by RIPK1 non-ubiquitylation due to depletion of cIAPs. The Pro-caspase 8 homodimer in complex IIa and complex IIb generates active Caspase 8. This active Caspase 8 in the cytosol then carries out cleavage reactions to activate downstream executioner caspases and thus induce classical apoptosis[1][2]. 

 

Reference:

[1]. Thomas C, et al. Caspases in retinal ganglion cell death and axon regeneration. Cell Death Discovery volume 3, Article number: 17032 (2017).
[2]. Brenner D, et al. Regulation of tumour necrosis factor signalling: live or let die. Nat Rev Immunol. 2015 Jun;15(6):362-74.

Caspase Isoform Comparison

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