bcl-2/bax

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

Bcl-2-IN-14 (Compound 13c), a BCL-2 inhibitor, exhibits an inhibitory concentration (IC 50) of 0.471 μM, and is applicable in cancer research [1].

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

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

Bcl-2-IN-5 is a potent inhibitor of BCL-2, demonstrating 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. Additionally, it effectively suppresses cell growth in Bcl 2-G101V knock-in RS4;11 cells, with IC50 values of 0.2 nM and 0.44 nM.

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].

Bcl-2-IN-13 is a potent inhibitor of Bcl-2, exhibiting an IC50 of 17 nM, and holds potential for use in cancer research [1].

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 Mcl-1 and Bcl-2 dual inhibitor.

Bcl-2-IN-9 is a novel, pro-apoptotic, low cytotoxic Bcl-2 inhibitor (IC50: 2.9 μM). Bcl-2-IN-9 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-3 is a Bcl-2/Mcl-1 inhibitor that acts on Mcl-1 (Ki: 0.14 μM) and Bcl-2 (Ki: 0.23 μM) and can be used in cancer research.

Bcl-2/Mcl-1-IN-2 is a Bcl-2 (Ki: 4.70 μM) and Mcl-1 (Ki: 0.88 μM) inhibitor.Bcl-2/Mcl-1-IN-2 can be used in cancer research.

MCL-1/BCL-2-IN-2 is a selective Mcl-1 and Bcl-2 inhibitor with potential antitumor activity for tumor 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.

MCL-1/BCL-2-IN-3 is a selective and potent Mcl-1 and Bcl-2 dual inhibitor with IC50s of 5.95 and 4.78 μM, respectiely.

MCL-1/BCL-2-IN-2 (Compound Nap-1) is a potent and selective dual inhibitor of Mcl-1 and Bcl-2 with IC 50 s of 4.45 and 3.18 μM, respectively [1].

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

Bcl-2-IN-11 (compound 6) is a potent and selective inhibitor of Bcl-2 activity, exhibiting an IC50 of 0.9 nM, and demonstrates minimal inhibition against Bcl-xl (IC50 > 1000 nM). This compound is utilized in researching various cancers linked to the overexpression of Bcl-2 family proteins, primarily malignant hematologic conditions such as acute lymphoid leukemia. Importantly, Bcl-2-IN-11 minimizes the risk of toxic side effects, including thrombocytopenia [1], by sparing Bcl-xl.

Bcl-2-IN-2 is a highly potent and selective inhibitor targeting Bcl-2 and Bcl-xL. It displays an IC50 value of 0.034 nM, suggesting its strong inhibitory activity specifically against Bcl-2. Additionally, Bcl-2-IN-2 exhibits an IC50 value of 43 nM against Bcl-xL, demonstrating over 1000-fold selectivity for Bcl-2 compared to Bcl-xL.

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

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.

Procyanidin C1 is a natural product, with anti-inflammatory effects, and induces apoptosis.

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.

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.

ABT-737 is a BH3 mimetic inhibitor of Bcl-xL, Bcl-2 and Bcl-w (EC50s: 78.7/30.3/197.8 nM).

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.

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

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

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.

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.

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

Physapubenolide is natural cytotoxic withanolide antitumor agent. Physapubenolide induces apoptosis by decreasing mitochondrial membrane potential and elevating the Bax/Bcl-2 protein expression ratio.

Dehydrocavidine (Dehydrocorydaline) has antitumor activity, it inhibits MCF-7 cell proliferation by inducing apoptosis mediated by regulating Bax/Bcl-2, activating caspases as well as cleaving PARP.

9(E),11(E),13(E)-Octadecatrienoic acid (β-ESA) is a conjugated polyunsaturated fatty acid that is found in plant seed oils and in mixtures of conjugated linolenic acids synthesized by the alkaline isomerization of linolenic acid. It reduces growth of Caco-2 colon cancer cells in a dose-dependent and time-dependent manner. In vitro, β-ESA induces DNA fragmentation and upregulation of pro-apoptotic Bax mRNA. β-ESA decreases protein expression of the apoptosis suppression factor Bcl-2 and induces apoptosis in T24 bladder cancer cells via production of reactive oxygen species. It also inhibits bacterial fatty acid dioxygenase with a Ki value of 49 nM in vitro.

BAX-IN-1 is a potential selective inhibitor of Bcl-2-associated X protein (BAX).

Ginsenoside Rg6 can inhibit JK cell proliferation in human lymphocytoma and induce its apoptosis, the mechanism may through mitochondrial dysfunction and an increase of Bax expression and decrease of Bcl-2 expression.

Wilfortrine can induce liver cancer cell HepG2 apoptosis, but with no effect on the cell cycle, mainly by promoting Bax expression and inhibiting anti-apoptotic protein Bcl-2 expression.

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.

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.

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.

BAI1 (Bax channel blocker) is a potent inhibitor of Bax-mediated mitochondrial cytochrome C release (IC50: 0.52 μM).

1. Dehydrocorydaline(DHC) not only inhibits antibody-mediated allergic reactions but also influences cell-mediated allergic reactions, and the inhibitory effect of Corydalis Tuber on allergic reactions may be partially attributed to DHC. 2. Dehydrocorydal

VDR agonist 1 (compound 28), a nonsteroidal Vitamin D receptor (VDR) agonist, demonstrates potent activity with a low IC 50 of 690 nM in MCF-7 cells. It inhibits cell cycle progression through upregulation of p21 and p27, and induces apoptosis by elevating BAX expression while reducing Bcl-2 levels [1].

Antitumor agent-37 exhibits potent anti-proliferative and anti-metastatic effects. antitumor agent-37 induces severe DNA damage, leading to high expression of γ-H2AX and p53. antitumor agent-37 induces apoptosis by exploiting the mitochondrial apoptosis pathway Bcl-2/Bax/caspase3. Antitumor agent-37 inhibits PD-L1 expression, increases CD3+ and CD8+ T-infiltrating cells in tumour tissue and significantly improves the immune response.

Asperosaponin VI (Akebia saponin D) , the most abundant constituent of the rhizome of Dipsacus asper, has been used for the treatment of lower back pain, traumatic hematoma and bone fractures.

CDK1/2/4-IN-1 (compound 3a) is a potent inhibitor of CDK with IC 50 values of 1.47, 0.78 and 0.87 μM for CDK1, CDK2 and CDK4, respectively. CDK1/2/4-IN-1 can be used in cancer research. CDK1/2/4-IN-1 arrests cell cycle at G2/M phase and induces apoptosis. CDK1/2/4-IN-1 elevates the level of Bax, caspase-3, and P53 and decreases the level of Bcl-2 [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.