1. Signaling Pathways
  2. Apoptosis
  3. Caspase

Caspase

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 1

  • Caspase 2

  • Caspase 3

  • Caspase 4

  • Caspase 5

  • Caspase 6

  • Caspase 7

  • Caspase 8

  • Caspase 9

  • Caspase 10

  • Caspase 12

  • Caspase

  • Caspase 11

Cat. No. Product Name Effect Purity
  • HY-16658
    Z-VAD(OMe)-FMK Inhibitor 98.20%
    Z-VAD(OMe)-FMK is a cell-permeable and irreversible pan-caspase inhibitor.
  • HY-13205
    Belnacasan Inhibitor 99.99%
    Belnacasan (VX-765) is an orally bioactive prodrug of VRT-043198, which is a potent and selective inhibitor of IL-converting enzyme (ICE)/caspase-1 with Kis of 0.8 nM and less than 0.6 nM for caspase-1 and caspase-4, respectively. Belnacasan (VX-765) inhibits the release of LPS-induced IL-1β and IL-18 by human PBMCs with an IC50 of ~0.7 μM.
  • HY-12305
    Q-VD-OPh Inhibitor 99.26%
    Q-VD-OPh is an irreversible pan-caspase inhibitor with potent antiapoptotic properties; inhibits caspase 7 with an IC50 of 48 nM and 25-400 nM for other caspases including caspase 1, 3, 8, 9, 10, and 12. Q-VD-OPh is able to cross the blood-brain barrier.
  • HY-12466
    Z-DEVD-FMK Inhibitor >98.0%
    Z-DEVD-FMK is a specific and irreversible caspase-3 inhibitor with IC50 of 18 μM.
  • HY-101297
    Z-IETD-FMK Inhibitor >98.0%
    Z-IETD-FMK is a selective and cell permeable caspase 8 inhibitor.
  • HY-19696B
    Tauroursodeoxycholate dihydrate Inhibitor
    Tauroursodeoxycholate dihydrate (TUDCA dihydrate; UR 906 dihydrate; Taurolite dihydrate) 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.
  • HY-107738
    Guggulsterone Activator 99.50%
    Guggulsterone is a plant sterol derived from the gum resin of the tree Commiphora wightii. Guggulsterone inhibits the growth of a wide variety of tumor cells and induces apoptosis through down regulation of antiapoptotic gene products (IAP1, xIAP, Bfl-1/A1, Bcl-2, cFLIP and survivin), modulation of cell cycle proteins (cyclin D1 and c-Myc), activation of caspases and JNK, inhibition of Akt. Guggulsterone, a farnesoid X receptor (FXR) antagonist, decreases CDCA-induced FXR activation with IC50s of 17 and 15 μM for Z- and E-Guggulsterone, respectively.
  • HY-N6979
    Crustecdysone Inhibitor 99.64%
    Crustecdysone (20-Hydroxyecdysone) is a naturally occurring ecdysteroid hormone isolated from Cyanotis arachnoides C.B.Clarke which controls the ecdysis (moulting) and metamorphosis of arthropods, it inhibits caspase activity and induces autophagy via the 20E nuclear receptor complex, EcR-USP. Crustecdysone exhibits regulatory or protective roles in the cardiovascular system.
  • HY-19696A
    Tauroursodeoxycholate Sodium Inhibitor
    Tauroursodeoxycholate Sodium 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.
  • HY-P1001
    Ac-DEVD-CHO Inhibitor 98.84%
    Ac-DEVD-CHO is a specific Caspase-3 inhibitor with a Ki value of 230 pM.
  • HY-10396
    Emricasan Inhibitor 99.88%
    Emricasan (PF 03491390) is an irreversible pan-caspase inhibitor.
  • HY-13523
    PAC-1 Activator
    PAC-1 is an activator of procaspase-3 induces apoptosis in cancer cells with EC50 of 2.08 μM.
  • HY-N0605
    Ginsenoside Rh2 Activator >98.0%
    Ginsenoside Rh2 is isolated from the root of Ginseng. Ginsenoside Rh2 induces the activation of caspase-8 and caspase-9. Ginsenoside Rh2 induces cancer cell apoptosis in a multi-path manner.
  • HY-N2027
    Taurochenodeoxycholic acid Activator 99.80%
    Taurochenodeoxycholic acid is one of the main bioactive substances of animals' bile acid.
  • HY-B1193
    Terfenadine Activator 98.26%
    Terfenadine ((±)-Terfenadine) is a potent open-channel blocker of hERG with an IC50 of 204 nM. Terfenadine, an H1 histamine receptor antagonist, acts as a potent apoptosis inducer in melanoma cells through modulation of Ca2+ homeostasis. Terfenadine induces ROS-dependent apoptosis, simultaneously activates Caspase-4, -2, -9 and induces p73, Noxa.
  • HY-13229
    BOC-D-FMK Inhibitor
    Boc-D-FMK is a cell-permeable, irreversible and broad spectrum caspase inhibitor; inhibits apoptosis stimulated by TNF-α with an IC50 of 39 µM.
  • HY-103667
    2-HBA Activator 98.83%
    2-HBA is a potent inducer of NAD(P)H:quinone acceptor oxidoreductase 1 (NQO1) which can also activate caspase-3 and caspase-10.
  • HY-15079
    Talampanel Inhibitor 98.59%
    Talampanel (LY300164) is an orally and selective α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor antagonis with anti-seizure activity. Talampanel (IVAX) has neuroprotective effects in rodent stroke models. Talampanel attenuates caspase-3 dependent apoptosis in mouse brain.
  • HY-10397
    EP1013 Inhibitor
    EP1013 is a broad-spectrum caspase selective inhibitor, used in the research of type 1 diabetes.
  • HY-N0905
    Ginsenoside Rh4 Activator 99.28%
    Ginsenoside Rh4 is a rare saponin obtained from Panax notoginseng. Ginsenoside Rh4 activates Bax, caspase 3, caspase 8, and caspase 9. Ginsenoside Rh4 also induces autophagy.

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.

Targets/MCE-Caspase-Signaling-Pathway.png

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.

Isoform Specific Products

Your Search Returned No Results.

Sorry. There is currently no product that acts on isoform together.

Please try each isoform separately.