apoptotic

K145 hydrochloride is a selective sphk2 inhibitor with substrate competitiveness and oral activity, with IC50 of 4.3 µM and Ki of 6.4 µM. K145 hydrochloride can induce apoptosis and has strong antitumor activity.

NSC-37445 has anti-tumor activity, such as inhibits growth of bladder tumor cells in a nude mice model , prevents the recurrence and progression of non-muscle-invasive urothelial cell carcinoma. NSC-37445 can significantly reduce the expression of CDK1-inhibitory kinases, Myt1 and Wee1, and cause cyclin B1 protein accumulation leading to CDK1 activation in T24 cells. 3. Flavokawain A (Flavokavain A) may exert anti-inflammatory responses by suppressing LPS-induced expression of pro-inflammatory mediators via blockage of NF-κB-AP-1-JNK/p38 MAPK signaling pathways in the murine macrophages.

PIK-75 hydrochloride (PIK-75 HCl) is a p110α inhibitor with IC50 of 5.8 nM (200-fold more potently than p110β), isoform-specific mutants at Ser773, and also potently inhibits DNA-PK with IC50 of 2 nM in cell-free assays.

PIK-75, a DNA-PK and PI3K inhibitor, suppresses DNA-PK(IC50=2 nM), p110α(IC50=5.8 nM) and p110γ(IC50=76 nM).

Adenosine amine congener (ADAC) (ADAC) is an agonist of selective A1 adenosine receptor,.

L-732138 is a potent and competitive antagonist of neurokinin-1 (NK-1) receptor(IC50 : 2.3 nM)

TC11 (1H-Isoindole-1,3(2H)-dione, 5-amino-2-[2,6-bis(1-methylethyl)phenyl]-TC11) is a potent inhibitor of tumor cell proliferation and an inducer of apoptosis via activation of caspase-3, 8 and 9.

Kea1-97 is a selective disruptor of interaction between thioredoxin and caspase-3 (IC50 = 10 μ M). Kea1-97 destroys the interaction between thioredoxin and caspase 3 and activates caspases without affecting the activity of thioredoxin.

Pinoresinol ((+)-Pinoresinol) has antiinflammatory, hepatoprotective, and fungicidal activities, it can protect pial microcirculation from I-reperfusion injury, to increase nitric oxide release and to reduce oxidative stress preserving pial blood flow distribution; it may exert pharmacologically interesting effects via modulation of the insulin-like signalling pathway in C.elegans. Pinoresinol causes an upregulation of the CDK inhibitor p21(WAF1/Cip1) both at mRNA and protein levels, inhibits NF-kappaB and activating protein 1 (AP-1).

Apoptotic agent-5 (5d) is an apoptosis-inducing factor that inhibits the growth of triple-negative breast cancer cells. It reduces proteasomal degradation through the ubiquitin-proteasome pathway, causing G2/M phase cell cycle arrest and triggering apoptosis (apoptotic).

Apoptotic agent-4 (Compound 9) is an apoptosis inducer. It inhibits VEGFR-2 with an IC50 of 0.5717 μM. Apoptotic agent-4 also suppresses the proliferation of cancer cells, causing cell cycle arrest in the G2/M and Pre-G1 phases.

Apoptotic agent-1 (Compound 8a) induces over-expression of the Fas receptor and Cyto C genes, exhibiting high antiproliferative activity against cancer cells and low cytotoxic effects [1].

Apoptotic agent-2 is capable of downregulating Bcl-2 and upregulating Bax and caspase-3 to induce apoptosis, exhibiting anti-proliferative effects that can be used in cancer research.

Apoptotic agent-3 utilizes a potential mitochondrial-mediated Bcl-2/Bax pathway and activates the caspase-3 pathway to promote apoptosis, exhibiting anti-proliferative effects that can be used to study cancer.

The compound, tumor-targeted pro-apoptotic peptide (CNGRC-GG-D(KLAKLAK)2), functions as an anti-tumor agent by disrupting mitochondrial membranes to induce apoptosis, demonstrating anticancer efficacy in mice [1].

RGD-Targeted Proapoptotic Peptide is a peptide that preferentially binds to integrins at sites of tumor angiogenesis through its C-terminal RGD-4C sequence (ACDCRGDCFC).

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.

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.

CK2/ERK8-IN-1 (TMCB) is a dual inhibitor of casein kinase 2 (CK2) (Ki: 0.25 µM) and ERK8 (IC50s: 0.50 μM) with pro-apoptotic efficacy. CK2/ERK8-IN-1 also binds to PIM1, DYRK1A, and HIPK2 (Kis: 8.65 µM, 11.9 µM, and 15.25 µM).

HLY78 (4-Ethyl-5-methyl-5,6-dihydro-[1,3]dioxolo[4,5-j]phenanthridine) targets the DIX domain of Axin, is an activator of the Wnt/β-catenin signaling pathway and can enhance Axin-LRP6 binding to promote Wnt signaling.

(S)-Thalidomide ((S)-(-)-Thalidomide) is the S-isomer of Thalidomide with immunomodulatory, anti-inflammatory, anticancer, anti-angiogenic, and pro-apoptotic activities, used in studying leprosy erythema nodosum and myeloma.

Sulfo-ara-F-NMN is an analogue of nicotinamide mononucleotide (NMN) with cellular permeability. Sulfo-ara-F-NMN was selective to activate SARM1 and inhibited CD38 with an IC50 of about 10 μM. Activation by Sulfo-ara-F-NMN to Z-48 or NMN, which has a higher cyclase activity, causes conformational changes in SARM1, resulting in cADPR production, NAD depletion, and non-apoptotic cell death.

TASIN-1 Hydrochloride (TASIN-1 HCl) is a selective inhibitor of truncated APC that acts by selectively killing colorectal cancer cells that express truncated APC by reducing cellular cholesterol levels and inducing apoptotic cell death through the ER stress/ROS/JNK signaling in colon cancer cells.