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-149800
    PARP-1-IN-3
    		Inducer 99.80%
    PARP-1-IN-3, a benzamide derivative, is a potent PARP-1 inhibitor with IC50 values of 0.25 nM and 2.34 nM for PARP-1 and PARP-2, respectively. PARP-1-IN-3 induces apoptosis and arrest cell cycle at G2/M phase. PARP-1-IN-3 can be used in research of cancer.
    PARP-1-IN-3
  • HY-130326
    RAPTA-C
    		Activator 99.30%
    RAPTA-C (Ru(η6-p-cymene)Cl2(pta)) acts as an anti-cancer and anti-angiogenic agent. RAPTA-C exhibits anti-metastatic, anti-angiogenic, and anti-tumoral activities through protein and histone-deoxyribonucleic acid alterations. RAPTA-C exhibits cell growth inhibition by triggering G(2)/M phase arrest in cancer cells. RAPTA-C also enhances the levels of p53 and triggers the mitochondrial Apoptotic pathway, resulting in cytochrome C release and caspase-9 activation. RAPTA-C reduces the growth of tumors with the inhibition of angiogenesis in a ovarian carcinoma model.
    RAPTA-C
  • HY-P2616A
    Mca-YVADAP-Lys(Dnp)-OH TFA
    		Chemical 98.29%
    Mca-YVADAP-Lys(Dnp)-OH TFA is a fluorogenic substrate for caspase-1 and angiotensin-converting enzyme 2 (ACE2).
    Mca-YVADAP-Lys(Dnp)-OH TFA
  • HY-131204
    CZL80
    		Inhibitor 98.31%
    CZL80, a brain-penetrable caspase-1 inhibitor with an IC50 of 0.01 μM, could be used in the study of febrile seizures and later enhanced epileptogenic susceptibility.
    CZL80
  • HY-B0835
    Fenobucarb
    		Activator 98.62%
    Fenobucarb is a carbamate insecticide. Fenobucarb induces zebrafish developmental neurotoxicity through pathways involved in inflammation, oxidative stress, degeneration and apoptosis. Fenobucarb is a possible risk factor to cardiovascular and cerebrovascular systems in animals.
    Fenobucarb
  • HY-W177546
    CD00509
    		Agonist 98.0%
    CD00509 is a tyrosyl-DNA phosphodiesterase (PDE) Tdp1 inhibitor with an IC50 of 0.71 μM. CD00509 increases DNA damage and promotes apoptosis of MCF-7 cells. CD00509 can sensitize breast cancer cells and wild-type murine embryonic fibroblasts (MEFs) to Camptothecin (CPT) (HY-16560). CD00509 can be used for the study of cancers such as breast cancer.
    CD00509
  • HY-131113
    N-Nitrosodibutylamine
    		99.93%
    N-Nitrosodibutylamine (N-Nitroso-di-n-butylamine) is a nitrosamine enriched in the drinking water. N-Nitrosodibutylamine regulates caspase pathway. N-Nitrosodibutylamine induces Apoptosis. N-Nitrosodibutylamine induces hepatocarcinoma and oxidative DNA damage.
    N-Nitrosodibutylamine
  • HY-147929
    Apoptotic agent-3
    		Activator 98.19%
    Apoptotic agent-3 (compound 15f) promotes apoptosis through the potential mitochondria-mediated Bcl-2/Bax pathway and activation of the Caspase 3 pathway. Apoptotic agent-3 exhibits anti-proliferative activities and can be used for cancer research.
    Apoptotic agent-3
  • HY-12546
    Brevetoxin B
    		Modulator
    Brevetoxin B (Brevetoxin-2) is a red tide toxin. Brevetoxin B affects sodium, potassium and calcium currents in nerve terminals. Brevetoxin B also modulates the metabolic activity of Jurkat cells, reduces cell viability and induces apoptosis. Brevetoxin B can be used in research on synaptic transmission and tumors.
    Brevetoxin B
  • HY-N3001
    Isolinderalactone
    		Activator 98.79%
    Isolinderalactone is a sesquiterpene that exhibits anti-cancer, anti-inflammatory, and neuroprotective effects. Isolinderalactone inhibits VEGF expression and tyrosine phosphorylation of VEGFR2. Isolinderalactone decreases viability and induces apoptosis in U-87 glioblastoma (GBM) cells and colorectal cancer (CRC) cells. Isolinderalactone induces G2/M phase cell cycle arrest, ROS generation, pJNK/p38 MAPK activation, in colorectal cancer (CRC) cells. Isolinderalactone blocks LPS (HY-D1056)-induced NF-κB activation while activating Nrf2-HMOX1 signaling in RAW264.7 macrophages. Isolinderalactone improves cognitive dysfunction in APP/PS1 mice. Isolinderalactone can be used for the study of Glioblastoma multiforme (GBM), colorectal cancer, Alzheimer’s disease and acute lung injury.
    Isolinderalactone
  • HY-N12717
    Casuarinin
    		Inhibitor 98.24%
    Casuarinin is an orally active antiproliferative, anti-inflammatory, antifungal, virucidal and gastroprotective agent. Casuarinin upregulates the expression of p21/WAF1, Fas/APO‑1, mFasL, sFasL and HSP‑70, arrests cell cycle, induces apoptosis and inhibits cancer cell proliferation. Casuarinin inhibits TNF‑α-induced phosphorylation of MAPK and activation of NF‑κB, downregulates the expression of iNOS, NF‑κB, COX‑2 and ICAM‑1, and reduces the production of proinflammatory mediators. Casuarinin attenuates ethanol-induced activation of caspase‑3 and elevation of TNF‑α, inhibits the growth of Candida albicans, and inhibits HSV‑2. Casuarinin can be used in research related to mammary adenocarcinoma, inflammatory skin diseases, gastric ulcers, candidiasis and herpes simplex virus infections.
    Casuarinin
  • HY-P2717
    Ac-YVAD-AMC
    		Inhibitor 99.64%
    Ac-YVAD-AMC is an inhibitor for caspase. Ac-YVAD-AMC inhibits bacteria-induced cell death of hypersensitive response (HR) cells.
    Ac-YVAD-AMC
  • HY-N5073
    Vitexin-4''-O-glucoside
    		Inhibitor 99.86%
    Vitexin-4''-O-glucoside (4''-O-Glucosylvitexin) is an orally active natural flavonoid component with multiple pharmacological effects including antioxidation, anti-inflammation, cytoprotection and anti-apoptosis. Vitexin-4''-O-glucoside regulates the MAPK signaling pathway by downregulating the phosphorylation levels of JNK and p38, thereby blocking endoplasmic reticulum stress responses. Vitexin-4''-O-glucoside alleviates oxidative stress by reducing MDA content and upregulating the activities of SOD and CAT, attenuates inflammation by downregulating the expressions of inflammatory factors TNF-α, IL-1β and IL-6, and also reduces LDH release and inhibits caspase-3 activation. Vitexin-4''-O-glucoside effectively improves drug-induced acute liver injury and exerts significant protective effects against myocardial hypoxia/reoxygenation injury. Vitexin-4''-O-glucoside can be used in studies on acute liver injury, cardiovascular diseases and myocardial hypoxia-reoxygenation injury.
    Vitexin-4''-O-glucoside
  • HY-N1157
    Thevetiaflavone
    		Inhibitor 99.83%
    Thevetiaflavone could upregulate the expression of Bcl-2 and downregulate that of Bax and caspase-3.
    Thevetiaflavone
  • HY-151966
    TD1092
    		Activator 99.49%
    TD1092 is a pan-IAP degrader, degrades cIAP1, cIAP2, and XIAP. TD1092 activates Caspase 3/7, and promotes cancer cells apoptosis via IAP degradation. TD1092 inhibits TNFα mediated NF-κB pathway and reduces the phosphorylation of IKK, IkBα, p65, and p38. TD1092 can act as PROTAC, and is used for cancer research.
    TD1092
  • HY-W750342
    Tryptophol-d4
    		Inhibitor 99.97%
    Tryptophol-d4 (Indole-3-ethanol-d4) is the deuterium labeled Tryptophol (HY-W010155). Tryptophol is an aromatic alcohol and secondary metabolite produced by microorganisms. Tryptophol induces apoptosis and cleavage of caspase-8. Tryptophol inhibits Cunninghamella blakesleeana biofilm. Tryptophol has anti-phage infection, biofilm formation regulation, anti-inflammatory, hemolytic, sleep induction, temperature change, seizure susceptibility and immune regulation activities. Tryptophol is used in the research of African trypanosomiasis, sleep disorders, epilepsy.
    Tryptophol-d<sub>4</sub>
  • HY-111954
    (+)-Erinacin A
    		Activator 99.81%
    (+)-Erinacin A (Erinacine A) is a cyanoditerpenoid isolated from Hericium erinaceus with anticancer, anti-inflammatory and neuroprotective activities. (+)-Erinacin A can induce cancer cell death by activating extrinsic and intrinsic apoptosis pathways. (+)-Erinacin A can also inhibit the expression of NO synthase (iNOS) and the production of nitrotyrosine to exert inflammatory and neuroprotective effects, thereby reducing ischemic brain damage.
    (+)-Erinacin A
  • HY-19696S1
    Tauroursodeoxycholate-d4
    		Inhibitor 99.70%
    Tauroursodeoxycholate-d4 is 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>
  • HY-N6576
    Hellebrigenin
    		Activator 99.69%
    Hellebrigenin is an inhibitor that selectively targets the MAPK signaling pathway (ERK, p38, JNK) and XIAP, and can inhibit Akt expression and phosphorylation. Hellebrigenin can activate endogenous apoptosis pathways (such as mitochondrial membrane potential disruption, Caspase family activation, PARP cleavage), downregulate anti-apoptotic proteins (Bcl-2, Bcl-xL) and upregulate pro-apoptotic proteins (Bax, Bak). Hellebrigenin can also induce DNA double-strand breaks to activate the ATM pathway. Hellebrigenin can inhibit tumor cell proliferation and clone formation, and is mainly used in the study of oral squamous cell carcinoma, liver cancer and other cancers.
    Hellebrigenin
  • HY-100573A
    (E/Z)-Necrosulfonamide
    		Inhibitor 98.03%
    (E/Z)-Necrosulfonamide is a racemic compound of Necrosulfonamide (HY-100573). Necrosulfonamide is a MLKL and Gasdermin D (GSDMD) inhibitor, capable of separately inhibiting necroptosis and pyroptosis of cells. Necrosulfonamide does not affect the activation of upstream signals, but specifically inhibits the downstream executor oligomerization step. Necrosulfonamide reduces the expression of the key kinases NLRP3 and caspase-1 involved in necroptosis and pyroptosis, activate the Nrf2 pathway and the downstream antioxidant enzymes, and also downregulates a variety of inflammatory factors. Necrosulfonamide plays significant roles in various diseases such as neurodegenerative diseases (such as Parkinson’s disease), tissue damage and ischemia-reperfusion injury, inflammatory bowel disease, osteoarthritis and fracture repair, and hair loss by regulating two important programmed necrosis pathways.
    (E/Z)-Necrosulfonamide
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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