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-P1006
    Ac-DEVD-pNA
    		Substrate 99.70%
    Ac-DEVD-pNA is a ligand for caspase-3/-7 and related cysteine proteases.
    Ac-DEVD-pNA
  • HY-P1007
    Z-VEID-FMK
    		Inhibitor
    Z-VEID-FMK (Z-VE(OMe)ID(OMe)-FMK) is a selective and irreversible caspase-6 peptide inhibitor. Z-VEID-FMK alleviates the drug-induced augmentation of caspase-6 activity, DNA fragmentation, and cell apoptosis.
    Z-VEID-FMK
  • 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-N1423S
    Glycocholic acid-d4
    		Activator 99.92%
    Glycocholic acid-d4 is the deuterium labeled Glycocholic acid (HY-N1423). Glycocholic acid is a bile acid derivative. Glycocholic acid downregulates MDR1, Bcl-2, MRP1, MRP2 and FXR, upregulates Bax, p53, caspase-9, caspase-3, TGR5 and S1PR2. Glycocholic acid inhibits multidrug resistance and efflux pumps, induces mitochondrial apoptosis, and enhances chemosensitivity. Glycocholic acid modulates related bile acid receptor signaling. Glycocholic acid suppresses growth and conjugation of Enterobacteriaceae and increases their antibiotic susceptibility. Glycocholic acid can be used for the research of colon adenocarcinoma and cholangiocarcinoma (CCA).
    Glycocholic acid-d<sub>4</sub>
  • HY-Y0148
    10-Hydroxydecanoic acid
    		Inhibitor 99.77%
    10-Hydroxydecanoic acid (10-HDAA) is a saturated fatty acid derived from 10-hydroxy-trans-2-decenoic acid, which can be isolated from royal jelly. 10-Hydroxydecanoic acid exhibits various biological activities, including anti-inflammatory, insecticidal, anti-malarial, and anti-Leishmania properties, as well as enhancing antigen-specific immune responses. The anti-inflammatory effects of 10-Hydroxydecanoic acid are primarily mediated by inhibiting the activation of NF-κB and the translation of interferon regulatory factor 1 (IRF-1), which reduces the production of interleukin 6 (IL-6) and nitric oxide (NO) in inflammatory cells. Additionally, 10-Hydroxydecanoic acid alleviates neuroinflammatory responses through the p53-autophagy pathway and the p53-NLRP3 pathway. Finally, 10-Hydroxydecanoic acid enhances antigen-specific immune responses by promoting the effective uptake of antigens by microfold cells.
    10-Hydroxydecanoic acid
  • HY-N0334A
    (+)-Magnoflorine iodide
    		Inhibitor 99.74%
    (+)-Magnoflorine (α-Magnoflorine) iodide is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine iodide promotes Parkin/PINK1 -mediated mitochondrial autophagy, inhibits the activation of NLRP3/Caspase-1 pathway, regulates the intestinal microbiota, and exhibits significant anti-inflammatory and immunomodulatory activities. (+)-Magnoflorine iodide inhibits JNK and TLR4/NF-κB signaling pathways, activates Sirt1/AMPK pathway, alleviates neuronal oxidative stress and apoptosis. Magnoflorine upregulates miR-410-3p, inhibits HMGB1/NF-κB pathway, and has anti-tumor activity. (+)-Magnoflorine iodide also has significant antifungal activity.
    (+)-Magnoflorine iodide
  • HY-120019
    Ac-YVAD-CHO
    		Inhibitor 98.99%
    Ac-YVAD-CHO (L-709049) is a potent, reversible, specific tetrapeptide interleukin-lβ converting enzyme (ICE) inhibitor with mouse and human Ki values of 3.0 and 0.76 nM. Ac-YVAD-CHO is also a caspase-1 inhibitor. Ac-YVAD-CHO can suppress the production of mature IL-lβ.
    Ac-YVAD-CHO
  • HY-N3415
    Kumatakenin
    		Activator 99.31%
    Kumatakenin is an orally active apoptosis inducer and autophagy inhibitor, with a Kd value of 2.94 μM for mouse ATG5. Kumatakenin increases the activities of caspase-3, caspase-8 and caspase-9, thereby inducing caspase-dependent apoptosis in ovarian cancer cells. Kumatakenin reduces the expression of chemokines and pro-oncogenic factors in ovarian cancer cells, and inhibits M2 macrophage polarization. Kumatakenin inactivates TRIM65 function, reduces the expression and stability of FASN, and thus inhibits the proliferation, migration, invasion and tumor progression of esophageal cancer cells. Kumatakenin interacts with ATG5 to reduce its protein level, decrease LC3 level, and reduce the number of autophagosomes in the hippocampus. Kumatakenin binds to Eno3 to upregulate its expression, reduce the stability and expression level of IRP1 mRNA, inhibit ferroptosis, alleviate intestinal inflammation, and restore epithelial barrier function. Kumatakenin enhances the efficacy of antibiotics against pathogenic bacteria, inhibits SARS-CoV-2 replication, and reduces cytokine production. Kumatakenin is applicable to research related to ovarian cancer, esophageal cancer, depression and colitis.
    Kumatakenin
  • HY-W011641
    (±)-Naringenin
    		Agonist 99.83%
    (±)-Naringenin is an orally available anti-inflammatory agent that can regulate both acute and chronic inflammation responses, while also showing antioxidant, neuroprotective, liver-protective, and anti-cancer effects. (±)-Naringenin promotes vasodilation in endothelial cells by activating BKCa channels in muscle cells. It also exerts protective effects against experimental colitis by inhibiting Toll-like receptor 4/NF-κB signaling, making it useful in studies related to sepsis, fulminant hepatitis, fibrosis, and cancer research.
    (±)-Naringenin
  • HY-N0674A
    Dehydrocorydaline chloride
    		Activator 99.75%
    Dehydrocorydaline chloride (13-Methylpalmatine chloride) is an alkaloid that regulates protein expression of Bax, Bcl-2; activates caspase-7, caspase-8, and inactivates PARP. Dehydrocorydaline chloride elevates p38 MAPK activation. Anti-inflammatory and anti-cancer activities. Dehydrocorydaline chloride shows strong anti-malarial effects (IC50?=38 nM), and low cytotoxicity (cell viability?>?90%) using P. falciparum 3D7 strain.
    Dehydrocorydaline chloride
  • HY-N0912
    Rehmannioside D
    		Modulator 99.89%
    Rehmannioside D is an orally active Sirt7 modulator. Rehmannioside D upregulates Sirt7 expression, inhibits the level of acetylated p53, and blocks the activation of the p53 signaling pathway. Rehmannioside D alleviates liver injury, inflammatory response, collagen deposition and hepatocyte apoptosis. Rehmannioside D is applicable to research related to liver fibrosis.
    Rehmannioside D
  • HY-P99934
    Eftozanermin alfa
    		Agonist 98.86%
    Eftozanermin alfa (ABBV-621) is a tumor necrosis factor-related apoptosis-inducing ligand receptor (TRAIL-R) agonist. Eftozanermin alfa is a fusion protein consisting of a mutant immunoglobulin G1-Fc linked to 2 single-chain trimers of TRAIL. Eftozanermin alfa induces apoptosis in tumor cells by activation of death receptors (DR4 receptor and DR5 receptor) with Kds of 780 nM and 635 nM. Eftozanermin alfa can be used for the research of multiple solid and heme malignancies.
    Eftozanermin alfa
  • HY-B1839
    Fluazinam
    		Activator 99.36%
    Fluazinam is an orally active dinitroaniline fungicide. Fluazinam induces phosphorylation of JNK, activates p38 pathway, decreases Bcl-2, activates caspase-3, decreases complex I activity, increases Autophagy and Apoptosis. Fluazinam has strong antifungal activity against F. fujikuroi and B. maydis. Fluazinam has a negative impact on Brachydanio rerio and worker bees.
    Fluazinam
  • 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-N0576
    Solanesol
    		Inhibitor 98.0%
    Solanesol is an orally active aliphatic terpene alcohol. Solanesol is mainly found in tobacco and other Solanaceae plants. Solanesol induces HO-1 and Hsp70 expression, activates p38 and Akt signaling pathways, and inhibits Apoptosis (reduces caspase-3 and PARP cleavage). Solanesol has antioxidant, anti-inflammatory, and neuroprotective activities. Solanesol can be used in the research of Huntington's disease, alcoholic liver disease, chronic inflammatory pain, anxiety, Alzheimer's disease, and bipolar disorder.
    Solanesol
  • HY-P1092
    Ac-IEPD-AFC
    		99.97%
    Ac-IEPD-AFC is a substrate of Granzyme B.
    Ac-IEPD-AFC
  • HY-P1093
    Ac-LEHD-AFC
    		99.95%
    Ac-LEHD-AFC is a fluorescent substrate for caspase-9, can be used to assess the activity of caspase.
    Ac-LEHD-AFC
  • HY-W111581
    Copper(II) diethyldithiocarbamate
    		98.5%
    Copper(II) diethyldithiocarbamate (Diethyldithiocarbamic acid copper salt) is a Copper(II) and diethyldithiocarbamate coordination polymer. Copper(II) diethyldithiocarbamate binds tightly to NPL4 and induces its aggregation, disrupting the p97-NPL4-UFD1 pathway. Copper(II) diethyldithiocarbamate causes ubiquitinated proteins accumulation and impairs waste proteins degradation, thus resulting in cell apoptosis. Copper(II) diethyldithiocarbamate inhibits tumor growth in MDA-MB-231 xenograft mice models. Copper(II) diethyldithiocarbamate can be used for the research of cancer, such as breast cancer.
    Copper(II) diethyldithiocarbamate
  • HY-105930
    Lobaplatin
    		Inducer 98.0%
    Lobaplatin (D-19466) is a diastereometric mixture of platinum(II) complexe. Lobaplatin arrests cell cycle at G1 and G2/M phase. Lobaplatin induces apoptosis by increasing expressions of caspase and Bax, decreasing expression of Bcl-2. Lobaplatin can be used for research of cancer.
    Lobaplatin
  • HY-N6818
    5,​7,​4'-​Trimethoxyflavone
    		Activator 99.65%
    5,7,4’-Trimethoxyflavone can be isolated from the medicinal plant Kaempferia parviflora (KP). 5,7,4’-Trimethoxyflavone is a CFTR activator and EC50 is 64 μM. 5,7,4’-Trimethoxyflavone induces apoptosis, increases proteolytic activation of caspase-3, and degradation of ADP-ribose polymerase (PARP) protein. 5,7,4’-Trimethoxyflavone has antitumor activity. 5,7,4’-Trimethoxyflavone can be used to prevent skin aging and oxidative stress.
    5,​7,​4'-​Trimethoxyflavone
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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