bax/bcl-2

Bcl-xL antagonist 2 is an effective and selective antagonist of Bcl-xL with an IC50 of 91 nM and a Ki of 65 nM. Bcl-xL antagonist 2 induces apoptosis in cancer cells and can be used in studies about chronic lymphocytic leukemia and non-Hodgkin’s lymphoma.

Bcl-2-IN-7 is a potent inhibitor of Bcl-2 (b-cell lymphoma-2), which can downregulate the expression of Bcl-2, increase the expression of p53, Bax, caspase-7 mRNA, and induce cell cycle arrest and apoptosis in MCF-7 cells of breast cancer. Bcl2-IN-7 showed good antitumor activity against MCF-7 cells (IC50: 20.17 μM), LoVo cells (IC50: 22.64 μM), HepG2 cells (IC50: 45.57 μM) and A549 cells (IC50: 51.50 μM).

Bcl-2-IN-6 is a potent inhibitor of Bcl-2 (b-cell lymphoma-2) that downregulates Bcl-2 expression and increases the expression of p53, Bax, and caspase-7 mRNA. bcl-2-IN-7 induces cell cycle arrest and apoptosis in breast cancer MCF-7 cells. bcl-2-IN-7 acts on MCF-7 cells ( Bcl2-IN-7 showed good antitumor effects on MCF-7 cells (IC50: 20.91 μM), LoVo cells (IC50: 22.30 μM), HepG2 cells (IC50: 42.29 μM) and A549 cells (IC50: 48.00 μM).

MCL-1 BCL-2-IN-4 is a selective and potent dual inhibitor of Mcl-1 and Bcl-2.

Bcl-2-IN-16 is an inhibitor of Bcl-2 (B-cell lymphoma 2) [1].

Bcl-2-IN-9 is a novel, pro-apoptotic, low cytotoxic Bcl-2 inhibitor (IC50: 2.9 μM) that downregulates Bcl-2 expression, induces apoptosis in cancer cells, and exhibits high selectivity for leukemia cells.

Bcl-2-IN-4, an orally active and selective inhibitor of Bcl-2, demonstrates potent efficacy with an IC50 value of 1.5 nM and exhibits more than 200-fold selectivity over Bcl-xL (IC50 of 411 nM). Additionally, it effectively inhibits the proliferation of RS4;11 cells, achieving an IC50 of 2.7 nM.

Bcl-2 Mcl-1-IN-2 is an inhibitor of Bcl-2 [Ki: 4.70 μM] and Mcl-1 [Ki: 0.88 μM], suitable for use in cancer research.

Bcl-2 Mcl-1-IN-3 is a Bcl-2 Mcl-1 inhibitor, targeting Mcl-1 (Ki: 0.14 μM) and Bcl-2 (Ki: 0.23 μM), suitable for cancer research.

Bcl-2 Mcl-1-IN-4 (compound 20) acts as a dual inhibitor targeting Bcl-2 (Ki=0.49 μM) and Mcl-1 (Ki=0.51 μM). This compound effectively suppresses cancer cell proliferation and induces apoptosis in U937 cells. It is utilized in cancer research.

PROTAC Bcl-xL degrader-2, based on von Hippel-Lindau ligand, is a potent degrader of Bcl-xL (a Bcl-2 family member), demonstrating an IC 50 of 0.6 nM.

Compound 72-1, also known as BCL-xL BCL-2 ligand 1, serves as a ligand for BCL-xL and BCL-2 proteins. It can be tethered to an E3 ligase via a linker, facilitating the formation of PROTACs [1] [2].

Bcl-2-IN-12 (Compound 1) is a potent Bcl-2 inhibitor with an IC50 value of 6 nM, used in cancer research [1].

Bcl-2-IN-14 (Compound 13c), a BCL-2 inhibitor with an inhibitory concentration (IC50) of 0.471 μM, is applicable in cancer research [1].

MCL-1 BCL-2-IN-2 is a potent and selective dual inhibitor of Bcl-2 and Mcl-1.

Bcl-2-IN-5 is a potent BCL-2 inhibitor with inhibitory concentrations (IC50) of 0.12 nM, 0.14 nM, and 0.22 nM against wild type Bcl-2, Bcl-2 D103Y, and Bcl-2 G101V, respectively. It also suppresses cell growth in Bcl 2-G101V knock-in [RS4;11] cells, with IC50 values of 0.2 nM and 0.44 nM.

MCL-1 BCL-2-IN-3 is a selective and potent dual inhibitor of Mcl-1 and Bcl-2, with IC50 values of 5.95 and 4.78 μM, respectively.

Bcl-2-IN-8 is a potent anti-cancer agent that exhibits anti-proliferative effects on both drug-sensitive and drug-resistant cancer cells, inhibits cell migration in a dose-dependent manner, blocks the cell cycle in the G1 phase, and induces apoptosis. Bcl-2-IN-8 has shown research potential in [triple-negative breast cancer].

MCL-1 BCL-2-IN-2 (Compound Nap-1) is a potent and selective dual inhibitor of Mcl-1 and Bcl-2, with IC50 values of 4.45 μM and 3.18 μM, respectively [1].

Bcl-2-IN-17, a Bcl2 inhibitor, is utilized for researching diseases associated with the Bcl anti-apoptotic protein [1].

Bcl-2-IN-15 (Compound 13d) is a Bcl-2 inhibitor with an IC50 of 363 nM that impedes the proliferation of the NCI leukemia cancer cell line [1].

Bcl-2-IN-2 is a highly potent and selective inhibitor targeting Bcl-2 and Bcl-xL, displaying an IC50 value of 0.034 nM against Bcl-2 and 43 nM against Bcl-xL, demonstrating over 1000-fold selectivity for Bcl-2 compared to Bcl-xL.

Bcl-2-IN-11 (compound 6) is a potent and selective Bcl-2 activity inhibitor with an IC50 of 0.9 nM and minimal inhibition against Bcl-xl (IC50 > 1000 nM). It is used in cancer research related to Bcl-2 family protein overexpression, particularly in hematologic malignancies like acute lymphoid leukemia, while minimizing the risk of side effects such as thrombocytopenia [1] by sparing Bcl-xl.

Bcl-2-IN-13, a potent Bcl-2 inhibitor with an IC50 of 17 nM, shows promise for cancer research applications [1].

Bcl-2 Mcl-1-IN-1 is an inhibitor of Bcl-2 (Ki: 4.53 μM) and Mcl-1 (Ki: 1.19 μM), and can be used in cancer research.

Beclin1-Bcl-2 Interaction Inhibitor 1 effectively disrupts the binding of Beclin 1 to Bcl-2, and is utilized in cancer and neurodegeneration research [1].

Procyanidin C1 is a natural polyphenol that causes DNA damage, cell cycle arrest, and apoptosis induction. It reduces Bcl-2 protein levels and enhances the expression of BAX, caspase 3, and 9 in cancer cells.

Ethyl gallate (gallic acid ethyl ester) obviously decreases cell proliferation in MDA-MB-231 and MCF-7 cells in a dose- and time-dependent manner, exhibits cytotoxicity in a dose-dependent manner. Ethyl gallate can inhibit the abilities of invasion of breast cancer in vitro by inhibiting the mRNA levels of MMP-9 MMP-2, phosphorylation of Akt and protein expression of NF-κB and inhibits hydrogen peroxide signaling, may represent an alternative class of vasopressors for use in septic shock. Also, Ethyl gallate suppresses proliferation and invasion in human breast cancer cells by modulating the PI3K Akt pathway, which may contribute to inhibiting their downstream targets such as NF-κB p-65, Bcl-2 Bax, and mRNA levels of MMP-2 and MMP-9 in breast cancer cells, could be used as potential antioxidants with safe therapeutic application in cancer chemotherapy.

Amygdalin (Laetrile) has antifibrotic, antitumor, anti-inflammatory and analgesic effects, amygdalin joint HSYA could inhibit the degeneration of the endplate chondrocytes derived from intervertebral discs of rats induced by IL-1beta and better than the single use of Amygdalin or HSYA. Amygdalin induces apoptotic cell death in human DU145 and LNCaP prostate cancer cells by caspase-3 activation through down-regulation of Bcl-2 and up-regulation of Bax.

Tetraethylammonium chloride is a quaternary ammonium compound. It is a non-selective potassium channel blocker. It is a good substrate for organic cation transporter proteins and has antitumor properties.

(S)-10-Hydroxycamptothecin (10-HCPT) is a DNA topoisomerase I inhibitor used as a clinical therapeutic agent against hepatoma.

trans-Chalcone (Chalkone) is an aromatic ketone that forms the central core for a variety of important biological compounds, which are known collectively as chalcones.

Quinacrine dihydrochloride (Mepacrine dihydrochloride) is the dihydrochloride salt of the 9-aminoacridine derivative quinacrine with potential antineoplastic and antiparasitic activities.

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.

Vanillyl Alcohol (3-Methoxy-4-hydroxybenzyl alcohol) possesses anti-angiogenic, anticonvulsive, anti-inflammatory, anti-oxidant, neuroprotective, and anti-nociceptive activities. Vanillyl alcohol can effectively inhibit the cytotoxicity and improved cell viability in 1-methyl-4-phenylpyridinium (MPP+)-induced MN9D dopaminergic cells, it also can attenuate the elevation of reactive oxygen species (ROS) levels, decrease in the Bax Bcl-2 ratio and poly (ADP-ribose) polymerase proteolysis.

Erianin is a nature product extracted from Dendrobium chrysotoxum, has notable antitumour activity , can cause extensive tumour necrosis, growth delay. Erianin has antiangiogenic action by inhibiting endothelial metabolism in a JNK SAPK-dependent manner a

ABT-737 is a BH3 mimetic and an inhibitor of Bcl-2, Bcl-xL, and Bcl-w (EC50=30.3 nM 78.7 nM 197.8 nM). ABT-737 exhibits antitumor activity and anti-aging activity.

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.

Cynarin (1,5-Dicaffeoylquinic acid) has neuroprotective, and antioxidant effects, it can inhibition of GSK3β as well as the modulation of Bcl-2 Bax.

1. Ilexsaponin A (Ilexsaponin A1) shows protective effects on ischemia-reperfusion-induced myocardial injury through anti-apoptotic pathway.

Cimidahurinine can attenuate Doxorubicin (DOX)-induced cardiotoxicity in a dose-dependent manner with EC50 values of 45.79 uM; it protects against cardiotoxicity by decreasing reactive oxygen species (ROS) accumulation and downregulating apoptosis-related Bax/Bcl-2 proteins.

Ginsenoside F4 has inhibitory effect on human lymphocytoma JK cell by inducing its apoptosis, the mechanism is related to the mitochondrial dysfunction and the increase of Bax expression and decrease of Bcl-2 expression.

Antitumor agent-77 inhibits the growth and migration of cancer cells and has anticancer effects. antitumor agent-77 inhibits GPx-4 and enhances COX2-induced iron sagging. antitumor agent-77 activates the intrinsic apoptotic pathway (Bax-Bcl-2-caspase-3) in tumor cells and prevents tumor cell epithelialization. Antitumor agent-77 activates the tumour cell intrinsic apoptotic pathway (Bax-Bcl-2-caspase-3) and blocks the epithelial mesenchymal transition (EMT) process.

1. β,β-Dimethylacrylshikonin (Dimethylacrylshikonin) is a promising agent for developing an improved strategy for radiotherapy against tumors. (a) Injection of Dimethylacrylshikonin combined with IR treatment significantly suppressed tumor growth of the HCT-116 xenograft. (b) Dimethylacrylshikonin significantly suppressed the growth of H(22) transplantable hepatoma, and induced the activation of caspase-3 . (c) Dimethylacrylshikonin inhibited growth of gastric cancer SGC-791 cells by inducing ERK signaling pathway. 2. Dimethylacrylshikonin inhibits the proliferation of MCF-7 cells in vitro by inducing apoptosis through the downregulation of Bcl-2, upregulation of Bax and partial inactivation of the NF-κB pathway.

FGFR-IN-13 (compound III-30), an irreversible covalent inhibitor of the fibroblast growth factor receptor (FGFR), effectively modulates signaling through FGFR1 (IC 50 = 0.20 ± 0.02 nM) and FGFR4 (IC 50 = 0.40 ± 0.03 nM). It suppresses the expression of crucial proteins such as total-PARP and Bcl-2, while enhancing the expression of Cleaved-PARP and Bax in a dose-dependent manner. Notably, FGFR-IN-13 demonstrates considerable antitumor and oral activity [1].

Co-treatment with Tanshinone IIB (TSB) significantly inhibits the DNA laddering, cytotoxicity and apoptosis of rat cortical neurons induced by staurosporine in a concentration-dependent manner; TSB also suppresses the elevated Bax protein and decreased bc

Uncarinic acid E has anti-cancer activity, it induces apoptosis in HepG2 cells via accumulation of p53, alters the Bax/Bcl-2 ratio, and activates caspases, resulting in cytochrome c release from the mitochondria. A mixture of uncarinic acid E and 27-O-p-(

Antitumor agent-36 exhibits strong anti-proliferative and anti-metastasis capabilities, causing significant DNA damage that results in elevated levels of γ-H2AX and p53. It promotes tumor cell apoptosis via the mitochondrial apoptotic pathway involving Bcl-2/Bax/caspase3 and enhances immune response by inhibiting PD-L1 expression, thereby increasing CD3+ and CD8+ T cell infiltration in tumor tissues [1].