2. Signaling Pathways
  3. Apoptosis
  4. Caspase

Caspase

Caspase

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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-N2420
    Flavokawain A
    		Activator 99.93%
    Flavokawain A is a chalcone compound and an orally active inhibitor of PRMT5 and cytochrome P450. Flavokawain A has anti-inflammatory, anti-tumor, and immunomodulatory effects. Flavokawain A can inhibit the proliferation of tumor cells and induce apoptosis. Flavokawain A can be used in the research of diseases such as bladder cancer.
    Flavokawain A
  • HY-N6018
    Beta-Eudesmol
    		Activator 99.49%
    Beta-Eudesmol has anticancer and anti-inflammatory activities. Beta-Eudesmol can induce apoptosis. Beta-Eudesmol is a neostigmine antagonist. Beta-Eudesmol can antagonize neostigmine-induced neuromuscular failure. Beta-Eudesmol can be used in the study of sepsis diseases. Beta-Eudesmol is a sesquiterpene-like compound that can be extracted from the rhizome of Atractylodes lancea.
    Beta-Eudesmol
  • HY-P0034A
    Ac-DEVD-CMK TFA
    		Inhibitor 99.07%
    Ac-DEVD-CMK (Caspase-3 Inhibitor III) TFA is a selective and irreversible caspase-3 inhibitor. Ac-DEVD-CMK TFA significantly inhibits apoptosis induced by high levels of glucose or 3,20-dibenzoate (IDB; HY-137295). Ac-DEVD-CMK TFA can be used in a variety of experimental approaches to inhibit apoptosis.
    Ac-DEVD-CMK TFA
  • HY-136744
    Caspase-9 Inhibitor III
    		Inhibitor 99.00%
    Caspase-9 Inhibitor III (Ac-LEHD-cmk) is a caspase-9 inhibitor. Caspase-9 Inhibitor III exhibits protective effects on ischemia-reperfusion-induced myocardial injury.
    Caspase-9 Inhibitor III
  • HY-13721
    Phenoxodiol
    		Activator 99.89%
    Phenoxodiol (Idronoxil), a synthetic analog of Genestein, activates the mitochondrial caspase system, inhibits XIAP (an apoptosis inhibitor), and sensitizes the cancer cells to Fas-mediated apoptosis. Phenoxodiol also inhibits DNA topoisomerase II by stabilizing the cleavable complex. Phenoxodiol induces cell cycle arrest in the G1/S phase of the cell cycle and upregulates p21WAF1 via a p53 independent manner.
    Phenoxodiol
  • HY-N7000
    Perillyl alcohol
    		Activator
    Perillyl alcohol is an orally active monoterpene. Perillyl alcohol exhibits multiple activities such as analgesic, anti-inflammatory, anti-tumor, anti-angiogenic, and anti-nociceptive effects. Perillyl alcohol can induce apoptosis and cell cycle arrest in tumor cells.
    Perillyl alcohol
  • HY-W013579
    (S)-(+)-Carvone
    		Activator 99.26%
    (S)-(+)-Carvone is an orally active natural product. (S)-(+)-Carvone increases the activity of antioxidant enzymes (SOD, CAT) and ROS, reduces the levels of oxidative stress markers (MDA, AChE), reduces the secretion of proinflammatory cytokines (IL-1β, IL-4, IL-6, IL-10), and downregulates NLRP3. (S)-(+)-Carvone increases the activities of caspase-8, -9 and -3. (S)-(+)-Carvone induces apoptotic death. (S)-(+)-Carvone has antimanic-like effect, liver protection and anticancer activity against skin cancer. (S)-(+)-Carvone improves memory and arthritis.
    (S)-(+)-Carvone
  • HY-18696
    AMG-337
    		Inducer 99.42%
    AMG-337 is a potent, orally active, selective MET kinase inhibitor with IC50 values of 1, 1, 4.7, 5, 21.5, 1077 and >4000 nM of WT MET, H1094R MET, M1250T MET, HGF-stimulated pMET (PC3 cells) MET, V1092I MET, Y1230H MET, and D1228H MET, respectively. AMG 337 inhibits the phosphorylation of MET and downstream effectors in MET-amplified cancer cell lines, resulting in an inhibition of MET-dependent cell proliferation and induction of apoptosis.
    AMG-337
  • HY-N2071
    Cedrol
    		Activator 99.76%
    Cedrol is a potent competitive inhibitor of cytochrome P-450(CYP) enzyme. Cedrol plays an anticancer role by inducing cell cycle arrest and Caspase-dependent apoptosis. Cedrol acts as a neutrophil agonist that can desensitize cells to subsequent stimulation of N-formyl peptides. Cedrol prevents neuropathic pain caused by chronic contractile injury by inhibiting oxidative stress and inflammation. In addition, Cedrol has antibacterial, hair loss prevention and anti-anxiety properties.
    Cedrol
  • HY-W016412
    Coenzyme Q0
    		Inducer 99.88%
    Coenzyme Q0 (CoQ0) is a potent, oral active ubiquinone compound can be derived from Antrodia cinnamomea. Coenzyme Q0 induces apoptosis and autophagy, suppresses of HER-2/AKT/mTOR signaling to potentiate the apoptosis and autophagy mechanisms. Coenzyme Q0 regulates NFκB/AP-1 activation and enhances Nrf2 stabilization in attenuation of inflammation and redox imbalance. Coenzyme Q0 has anti-angiogenic activity through downregulation of MMP-9/NF-κB and upregulation of HO-1 signaling.
    Coenzyme Q0
  • HY-P1093
    Ac-LEHD-AFC
    		98.22%
    Ac-LEHD-AFC is a fluorescent substrate for caspase-9, can be used to assess the activity of caspase.
    Ac-LEHD-AFC
  • HY-14569
    CDPPB
    		Inhibitor 99.32%
    CDPPB is a selective, orally active mGluR5 allosteric modulator. CDPPB increases AKT and ERK1/2 activation and augments the BDNF mRNA. CDPPB inhibits caspase-3 activation and mitochondrial dysfunction. CDPPB improves cognitive impairment, depression, and Huntington's disease.
    CDPPB
  • HY-103667
    2-HBA
    		Activator 99.09%
    2-HBA is a potent inducer of NAD(P)H:quinone acceptor oxidoreductase 1 (NQO1) which can also activate caspase-3 and caspase-10.
    2-HBA
  • HY-P1986
    Z-DEVD-AFC
    		98.95%
    Z-DEVD-AFC is a cell-permeant substrate for caspase-3, which causes a shift in fluorescence uponcleavage of the AFC fluorophore. Z-DEVD-AFC can be used to detect caspase-3-like enzymes activity.
    Z-DEVD-AFC
  • HY-W011978
    N-Acetyl-L-tryptophan
    		Inhibitor 99.38%
    N-Acetyl-L-tryptophan is an antagonist of the neurokinin-1 receptor (NK-1R), disrupting the binding of substance P (SP) to NK-1R. This action provides neuroprotective effects, improving memory deficits and motor impairments. N-Acetyl-L-tryptophan is also an inhibitor of cytochrome c (Cytochrome c), and it exerts antioxidant and anti-inflammatory effects by inhibiting the expression of IL-1β and the activation of caspase-1. N-Acetyl-L-tryptophan holds promise for research in neurodegenerative and inflammatory diseases.
    N-Acetyl-L-tryptophan
  • HY-119459
    Fluopyram
    		Activator 99.33%
    Fluopyram is an orally active succinate dehydrogenase inhibitor, antifungal and nematicide. Fluopyram inhibits succinate dehydrogenase activity, activates CAR/PXR nuclear receptors, and increases caspase-3, TNF-α and NF-κB. Fluopyram inhibits the growth of F. virguliforme, Botrytis cinerea and Alternaria solani with EC50 values of 3.35, 5.389 and 0.244 µg/mL, respectively. Fluopyram induces liver and thyroid tumor formation. Fluopyram is nephrotoxic and embryotoxic.
    Fluopyram
  • HY-D0848
    N,N'-Methylenebisacrylamide
    		Activator 99.66%
    N,N'-Methylenebisacrylamide (Bisacrylamide) is an orally active acrylamide dimer and crosslinker. N,N'-Methylenebisacrylamide increases CYP2E1, P53, cleaved caspase-3. N,N'-Methylenebisacrylamide promotes hepatic cancer. N,N'-Methylenebisacrylamide changes sperm abnormality rate and sperm count. N,N'-Methylenebisacrylamide decreases the number of various cells in the blood as well as induces liver and testicular damage. N,N'-Methylenebisacrylamide is used to prepare polyacrylamide gel.
    N,N'-Methylenebisacrylamide
  • HY-P1006
    Ac-DEVD-pNA
    		Substrate 98.12%
    Ac-DEVD-pNA is a ligand for caspase-3/-7 and related cysteine proteases.
    Ac-DEVD-pNA
  • HY-N0809
    Sesamolin
    		Inhibitor 99.78%
    Sesamolin, isolated from Sesamum indicum, has antioxidative activity, Sesamolin inhibits lipid peroxidation and shows neuroprotection effect. Sesamolinl potently inhibits MAPK cascades by preventing phosphorylation of JNK, p38 MAPKs, and caspase-3 but not ERK-MAPK expression. Sesamolin is orally active.
    Sesamolin
  • HY-124832
    δ-Secretase inhibitor 11
    		Inhibitor 99.06%
    δ-Secretase inhibitor 11 (compound 11) is an orally active, potent, BBB-penetrated, non-toxic, selective and specific δ-secretase inhibitor, with an IC50 of 0.7 μM. δ-Secretase inhibitor 11 interacts with both the active site and allosteric site of δ-secretase. δ-Secretase inhibitor 11 attenuates tau and APP (amyloid precursor protein) cleavage. δ-Secretase inhibitor 11 ameliorates synaptic dysfunction and cognitive impairments in tau P301S and 5XFAD transgenic mouse models. δ-Secretase inhibitor 11 can be used for Alzheimer's disease research.
    δ-Secretase inhibitor 11
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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