cleaved caspase 3

CAY10526 (BTH) is a selective mPGES-1 inhibitor that acts as an inhibitor of the NF-κB signaling pathway.

Polyphyllin D induces apoptosis via the mitochondrial apoptotic pathway as evidenced by decreased Bcl-2 expression levels, disruption of MMP and increased Bax, cytochrome C, and cleaved-caspase-3 levels. Polyphyllin D has an anti-angiogenic effect. Polyphyllin D has toxicity in human RBCs as well as its underlying mechanism for the hemolysis and eryptosis/erythroptosis. Polyphyllin D has strong anticancer activity, can overcome drug resistance in R-HepG2 cells and elicit programmed cell death via mitochondrial dysfunction.

CSRM617 hydrochloride is a selective small-molecule inhibitor of the transcription factor ONECUT2 (OC2, a master regulator of androgen receptor), with a Kd of 7.43 µM in SPR assays, directly binding to the OC2-HOX domain. CSRM617 hydrochloride induces apoptosis through the appearance of cleaved Caspase-3 and PARP and is well tolerated in the mouse model of prostate cancer [1].

Emamectin Benzoate (MK-244), by binding gamma-aminobutyric acid (GABA) receptor and glutamate-gated chloride channels disrupting nerve signals within arthropods, acts as a chloride channel activator.

D-Isofloridoside, a polysaccharide precursor, exhibits free radical scavenging activity and inhibits both ROS expression and the enzymes MMP-2 and MMP-9.

EV206 is an effective inhibitor of Hsp70, exhibiting antiproliferative properties. This compound induces cell apoptosis (apoptosis) and enhances the protein expression of cleaved PARP and caspase-3. Additionally, EV206 demonstrates antitumor activity.

MAPK-IN-3 (Compound 4a) is an antiproliferative agent demonstrating significant inhibitory effects on KYSE 30, HCT 116, and HGC 27 cell lines, with IC50 values of 0.57 μM, 3.27 μM, and 2.28 μM, respectively. This compound arrests the cell cycle via a p53-dependent mechanism and induces apoptosis through a p53-independent pathway. It reduces the expression of cell cycle-related proteins, such as Cyclin D1 and Cyclin B1, while increasing pro-apoptotic proteins like cleaved PARP, cleaved caspase-7, and cleaved caspase-9. MAPK-IN-3 also decreases anti-apoptotic proteins such as Bcl-2, elevates ROS levels in KYSE 30 cells, and enhances the expression of ROS-related MAPK pathway members, including p-ERK, p-p38, and p-JNK.

TFGF-18 is a GSK-3β inhibitor with an IC50 of 0.59 μM. It suppresses microglial activation and the release of pro-inflammatory mediators induced by LPS by inhibiting GSK-3β and downstream p65/NF-κB signaling. TFGF-18 also prevents neuronal apoptosis and oxidative stress, reduces the expression of Bax, caspase-3, and cleaved-caspase-3, while increasing Bcl-2 expression. It offers neuroprotection by inhibiting neuroinflammation and alleviating cognitive impairment.

Bfl-1-IN-6 (Compound 20) is an orally active inhibitor of Bcl-2-related protein A1 (BFL1) with an IC50 of 19 nM. This compound can stabilize BFL1 protein, activate cleaved caspase 3, and demonstrates antitumor activity in mouse models.

FMP is a platinum (IV) complex. It significantly upregulates the expression of γ-H2AX and p53, enhances ROS production, and markedly increases the expression of apoptosis (Apoptosis) related proteins (DR5, Fas, caspase-8, Cyt-c, caspase-3, cleaved-PARP1, Bax). FMP exhibits antiproliferative activity against breast cancer.

DNH28 is a potent NF-κB and MAPK inhibitor with an IC50 value of 0.93 μM in HepG2 cells. It induces apoptosis by downregulating Bcl-2 and upregulating BAX and Cleaved-caspase-3 expression. DNH28 can arrest the cell cycle and inhibit cell migration, and is applicable for research in hepatocellular carcinoma (HCC).

(E)-3,4-Dimethoxycinnamic acid is a less active isomer of 3,4-dimethoxycinnamic acid, a natural monomer from Securidaca inappendiculata Hassk. It exerts anti-apoptotic effects in L-02 cells via ROS-mediated signaling, showing potential in research related to inflammation and immunology.

Downregulate phosphorylation of STAT3, increase the expression of cleaved caspase-3, inhibit cell cycle progression and promote apoptosis in breast and pancreatic cancer cells with low micromolar to nanomolar IC50 values. Furthermore, HJC-0123 significantly suppressed estrogen receptor (ER)-negative breast cancer MDA-MB-231 xenograft tumor growth in vivo (p.o.), indicating its great potential as an efficacious and orally bioavailable drug candidate for human cancer therapy.

Lig4-4 is a TREK-1 current inhibitor (IC50 = 2.06 μM) that has demonstrated potential for use as a protective agent against cerebral ischemia. It has been postulated that the neuroprotective effects of Lig4-4 against cerebral ischemia may be attributed to the modulation of Bcl-2 and cleaved-caspase-3 expression, leading to the inhibition of neuronal apoptosis.

Anticancer agent 137 (8q), a potent PI3k inhibitor, exhibits broad-spectrum anticancer activity by inducing G2/M cell cycle arrest and apoptosis. It increases levels of cleaved PARP, and caspases 3 and 7, making it useful in cancer research [1].

Myrothecine A, a trichothecene mycotoxin discovered in M. roridum, exhibits anticancer properties. It effectively inhibits the proliferation of various cancer cell lines, specifically A549, MCF-7, HepG2, and SMMC-7721, with IC50 values of 95, 70, 60, and 25 µM, respectively. At a concentration of 50 µM, Myrothecine A induces G1 cell cycle arrest in HepG2 cells and promotes apoptosis in SMMC-7721 cells by elevating levels of Bax and cleaved caspase-3, -5, and -8.

RPS6-IN-1 (Compound 22o) inhibits cell migration and induces apoptosis (increasing the expression of Bax, p53, cleaved-caspase 3, and cleaved-PARP). It reduces mitochondrial membrane potential and activates autophagy (Autophagy) through the PI3K-Akt-mTOR signaling pathway, damaging mitochondria and lysosomes within the cell and causing endoplasmic reticulum stress. RPS6-IN-1 also inhibits the phosphorylation of RPS6. Notably, RPS6-IN-1 is a low systemic toxicity anticancer agent.

Caspase-3 Activator 4 (compound 4o) is an effective caspase-3 activator that can cross the blood-brain barrier. This compound exhibits antiproliferative activity and can induce cell apoptosis (apoptosis). Additionally, Caspase-3 Activator 4 enhances the gene expression of TNF-α and reduces the expression of cleaved caspase-3/caspases 3.

Polyphyllin I (Standard) is a reference standard for research and analysis in studies involving Polyphyllin I. Polyphyllin D induces apoptosis via the mitochondrial apoptotic pathway as evidenced by decreased Bcl-2 expression levels, disruption of MMP and increased Bax, cytochrome C, and cleaved-caspase-3 levels. Polyphyllin D has an anti-angiogenic effect. Polyphyllin D has toxicity in human RBCs as well as its underlying mechanism for the hemolysis and eryptosis/erythroptosis. Polyphyllin D has strong anticancer activity, can overcome drug resistance in R-HepG2 cells and elicit programmed cell death via mitochondrial dysfunction.

Avenanthramide C is an orally available natural alkaloid with antioxidant/inflammatory properties that reduces the expression of TNF-a, BAK, IL-1b, and Bcl-2; reverses memory and behavioral deficits in Alzheimer's disease, with a reduction in caspase-3 cleavage and an increase in levels of pS9GSK-3β and IL-10, is able to bind α1A adrenergic and stimulate AMPK; can attenuate noise and drug-induced hearing loss.

Cell-permeable peptide cleaved from protease-activated receptor 1 (PAR1) upon receptor activation. Attenuates endothelial cell migration and proliferation (IC50 ~ 3 μM), and induces cell cycle arrest. Promotes activation of caspase-3 and exhibits pro-apop

Cell-permeable peptide cleaved from protease-activated receptor 1 (PAR1) upon receptor activation. Attenuates endothelial cell migration and proliferation (IC50 ~ 20 μM), and induces cell cycle arrest. Promotes activation of caspase-3 and exhibits pro-apo

Agkistrodon halys batroxobin is a thrombin-like serine protease. It reduces the expression of Sirt1 and the activation of extracellular signal-regulated kinase in brain tissue. Additionally, this compound decreases cleaved caspase-3 expression in rats, thereby inhibiting neuronal apoptosis (apoptosis).