caspase-dependent

KY-05009 is a chemical compound that effectively suppresses TGF-β1-induced epithelial-to-mesenchymal transition (EMT) in human lung adenocarcinoma cells, reduces TNIK protein expression and the transcriptional activity of Wnt target genes, and promotes apoptosis in cancer cells, displaying anti-cancer properties. Furthermore, it functions as an ATP-competitive Traf2- and Nck-interacting kinase (TNIK) inhibitor with a Ki of 100 nM.

PAF (C16) is a potent MAPK and MEK/ERK activator that induces increased vascular permeability. PAF (C16) (PAF (C16)) is a platelet-activating factor, a phospholipid-derived mediator and a ligand for PAF G protein-coupled receptor (PAFR). PAF (C16) has shown anti-apoptotic and anti-inflammatory activity in vitro, inhibiting Caspase-dependent apoptosis by interacting with its receptor (PAF-R) to perform cell signaling.

(-)-Anonaine can be extracted from several species of Magnoliaceae and Annelidae and has antimalarial, antibacterial, antifungal, antioxidant, anticancer, antidepressant and vasodilatory activities. (-)-Anonaine induces apoptosis in human cervical cancer (HeLa) cells, induces DNA damage and inhibits the growth and migration of human lung cancer h1299 cells through Bax and caspase-dependent pathways.

OUP-186 is a high affinity and human/rat species-selective antagonist of histamine H3 receptor. OUP-186 suppressed the proliferation of breast cancer cells. The IC50 values at 48 hours for OUP-186 was approximately 50 μM. OUP-186 potently induced cell dea

CIL62 is a Necrostatin-1 dependent inducer of cell death through a caspase-3/7-independent mechanism [1].

BJE6-106 (B106) is a selective PKCδ inhibitor (IC50 = 0.05 μM) with 1000-fold higher selectivity for PKCδ than PKCα (IC50 = 50 μM). BJE6-106 induces caspase-dependent apoptosis, activates the JNK pathway and H2AX, and can be used to study NRAS-mutated melanoma.

Destruxin B is a cyclic peptide with insecticidal and anticancer activity isolated from the insect pathogenic fungus Metarhizium isopliae. Destruxin B induces apoptosis of human non-small cell lung cancer cells through the Bcl-2 family-dependent mitochond

Eltanexor (ONO-7706) is an orally active exportin-1 (XPO1) inhibitor. It has effective anti-leukemic activity. Eltanexor inhibits XPO1-dependent nuclear export (EC50=60.9 nM) by directly targeting XPO1. Eltanexor causes caspase-dependent apoptosis in a panel of leukemic cell lines.

Mensacarcin, a highly complex polyketide compound, exhibits multifaceted effects on cellular processes. Specifically, it targets mitochondria, perturbs energy metabolism within these organelles, and activates caspase-dependent apoptotic pathways. Functionally, Mensacarcin can serve as a cytotoxic constituent in antibody-drug conjugates (ADCs). Furthermore, this antibiotic compound displays broad-spectrum inhibition of cell growth across various cancer cell lines and demonstrates potent induction of apoptosis in melanoma cells.

PETCM is a caspase-3 activator and acts as an cytochrome c (cyto c)-dependent manner.

15-Acetoxyscirpenol, a member of the acetoxyscirpenol moiety mycotoxins (ASMs), potently induces apoptosis and inhibits the growth of Jurkat T cells in a dose-dependent manner. This effect is mediated through the activation of caspases independent of caspase-3[1].

A-1155905 is an MCL-1 inhibitor with anticancer activity, demonstrating a half maximal inhibitory concentration (IC50) of 33.5 Nm and a dissociation constant (Ki) of 0.58 nM. This compound selectively binds to MCL-1 and possesses sufficient affinity to disrupt the MCL-1-Bim complex in live cells. The induction of death in MCL-1-dependent cell lines by A-1155905 is reliant on caspase proteins and occurs through apoptosis.

EGFR-IN-137 (Compound 4c) acts as an inhibitor of aromatase and EGFR, with IC50 values of 1.67 μg/mL and 0.08 μg/mL, respectively. It hinders the proliferation of cancer cells MCF-7 and MDA-MB-231, with IC50 values of 1.62 µM and 4.14 µM. Additionally, EGFR-IN-137 induces cell cycle arrest at the G0/G1 phase in MDA-MB-231 cells and triggers apoptosis through a caspase-dependent pathway.

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.

Apoptosisinducer 31 (compound 19) triggers caspase-dependent apoptosis (cell death). It plays a crucial role in cancer research.

ZIF-8 is an anticancer agent that can inherently trigger pyroptosis through a caspase-1/gasdermin D (GSDMD)-dependent pathway.

BJ-13 is a reactive oxygen species (ROS) inducer that causes mitochondrial membrane potential collapse and caspase-dependent apoptosis. It inhibits the proliferation of SGC-7901, U-87MG, and HepG-2 cancer cells with IC50 values of 15.33, 27.18, and 20.44 nM, respectively. BJ-13 is applicable in gastric cancer research.

BKT-300 is a potent and selective inhibitor of Protein regulator of cytokinesis 1 (PRC1), with a Kd value of 28.3 nM. It disrupts microtubule architecture, induces G2/M phase arrest, mitotic catastrophe, and caspase-3-dependent apoptosis, presenting potential as a novel therapy for advanced acute myeloid leukemia (AML).

GQN-B37-Me is an MCL-1 inhibitor that can induce caspase-dependent apoptosis. It exhibits significant cytotoxicity in H929 (IC50= 3.71 μM) and MV-4-11 (IC50= 5.57 μM) cell lines. GQN-B37-Me is useful for leukemia research.

NLRP3-IN-81 (N102) is an inhibitor capable of crossing the blood-brain barrier, effectively countering NLRP3 inflammasome-dependent pyroptosis with an EC50 of 0.029 μM for Nigericin-induced pyroptosis. It significantly suppresses caspase-1 activation and IL-1β release that depend on NLRP3. Additionally, NLRP3-IN-81 disrupts the interaction between NLRP3 and the adaptor protein ASC, while inhibiting ASC oligomerization. This compound is applicable in research on pyroptosis-related diseases, such as inflammatory bowel disease and type 2 diabetes.

FAK-IN-28 is an orally active FAK inhibitor with an IC50 of 0.4 nM. It exhibits both antiproliferative and antimetastatic effects. FAK-IN-28 induces apoptosis by triggering caspase-3-dependent pathways through increased ROS levels. This compound effectively inhibits tumor growth without causing weight loss or hepatorenal toxicity. FAK-IN-28 is suitable for research on FAK-driven malignancies, including colon cancer, cervical cancer, triple-negative breast cancer, and melanoma.

NLRP3 modulator 8 (Compound 14) is an NLRP3 regulator that can significantly degrade the NEK7 protein (DC50 = 9 nM). In macrophages, NLRP3 modulator 8 can inhibit the activity of caspase-1 in a dose-dependent manner and reduce the release of IL-1β triggered by the activation of the NLRP3 inflammasome. NLRP3 modulator 8 is applicable for the research of various diseases, including autoinflammatory and autoimmune diseases, neurodegenerative diseases, as well as cardiovascular and metabolic-related diseases, etc.

MMPSI (Caspase-3/7 Inhibitor I) is a novel, non-peptide small molecule caspase 3 and caspase 7 inhibitor that reduces ischemic injury in isolated rabbit heart or cardiomyocytes and inhibits apoptosis of H16c2 cells in a concentration-dependent manner.MMPSI can be used to study cardioprotection and myocardial injury.

PB28 dihydrochloride is a selective and potent sigma 2 (σ2) receptor agonist and σ1 receptor antagonist with anti-SARS-CoV-2 activity and anti-tumor activity, which inhibits cell proliferation and invasion and suppresses SKF by modulating the PI3K-AKT-mTOR signaling pathway in renal cancer. It inhibits cell proliferation and invasion by regulating the PI3K-AKT-mTOR signaling pathway in renal cancer, inhibits calcium release from the endoplasmic reticulum of SK-N-SH neuroblastoma cells, and induces non-caspase-dependent apoptosis.