bax activation

DD1 (HUN85111) is a proteasome inhibitor that induces human myeloid tumor-selective apoptosis.

1. Dehydrocorydaline (13-Methylpalmatine) exerts anti-metastatic potential via suppression of MMPs and Bcl-2 signaling in NSC-LC cells. 2. Dehydrocorydaline stimulates p38 MAPK activation, which can enhance heterodimerization of MyoD and E proteins, thus resulting in MyoD activation and myoblast differentiation. 3. Dehydrocorydaline shows antiplatelet effects, it inhibits thrombin-induced platelet aggregation in a low dose ( IC50= 34.914 ug/mL). 4. Dehydrocorydaline has anti-inflammatory and antinociceptive effects. 5. Dehydrocorydaline inhibits MCF-7 cell proliferation by inducing apoptosis mediated by regulating Bax/Bcl-2, activating caspases as well as cleaving PARP.

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.

Diphenyl disulfide (Phenyl disulfide) shows anticancer activity in breast cancer cell lines.Diphenyl disulfide induces and enhances apoptosis in breast cancer cells through Bax protein hydrolysis activation and concomitant autophagy.Diphenyl disulfide inhibits cell proliferation and viability and reduces colony formation in a dose-dependent manner. Diphenyl disulfide can be used to treat breast cancer.

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.

Dehydrocorydaline chloride (13-Methylpalmatine chloride) is an alkaloid exhibiting anti-inflammatory and anti-cancer activities and can enhance the activation of p38 MAPK.

BSO-07 is a ROS JNK activator that exhibits potent anti-cancer properties, demonstrated by an IC50 of 24.81 μM in human breast cancer (BC) cells. The mechanism of action for BSO-07 involves JNK activation and the promotion of increased ROS levels, which lead to the induction of apoptosis (Apoptosis) and tumorigenic apoptosis. This includes enhanced expression of apoptosis-related proteins such as PARP, Bax, phosphorylated p53, ATF4, and CHOP, along with a reduction in the levels of anti-apoptotic proteins (e.g., Bcl-2, Bcl-xL, and Survivin). BSO-07 holds promise for research in the field of breast cancer.

CBI1 formic is a covalent inhibitor of BAX, selectively derivatizing BAX at C126 and inhibiting its activation by triggering with a ligand or point mutation. This compound effectively blocks the t-2-hex lipidation and oligomerization of BAX. Additionally, CBI1 formic inhibits BAX activation induced by BH3 ligands, F116A mutations, or t-2-hex.

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.

Fraxetin (7,8-dihydroxy-6-methoxy coumarin) has dual-antioxidative ,hepatoprotective and antihyperglycemic functions, it shows potent protective effects against CCl4 induced oxidative stress and hepatic fibrosis, has a marked inhibitory effect on S.aureus proliferation. It increased the level of Nrf2/ARE, and HO-1, inhibit the formation of ROS, cytochrome c release, activation of caspase-3 and 9, and suppressed the up-regulation of Bax.

CG0009 is a potent and highly selective glycogen synthase kinase 3 (GSK3) inhibitor that inhibitions proliferation, induces apoptosis, and activates the p53-Bax pathway in breast cancer cells through cyclin D1 depletion. CG0009 inhibit breast cancer cell

Jaceosidin has anti-oxidative activity. Jaceosidin has anti-inflammatory activity, also a microglial inhibitor with anti-neuroinflammation activity. aceosidin has anticancer activity, modulates the ERK/ATM/Chk1/2 pathway, leading to inactivation of the Cd

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.

BTSA1 is a BAX activator that binds with high affinity and specificity to the N-terminal activation site and induces conformational changes to BAX leading to BAX-mediated apoptosis.

Anticancer agent 56 (compound 4d) is a powerful anti-cancer compound with favorable drug-like properties, showing significant anticancer activity against multiple cancer cell lines with an IC50 value of less than 3 μM. It exerts its effects by causing cell cycle arrest at the G2/M phase and activating the mitochondrial apoptosis pathway, inducing the accumulation of reactive oxygen species (ROS), upregulating BAX, downregulating Bcl-2, and triggering the activation of caspases 3, 7, and 9 [1].

Ipatasertib (GDC-0068) is a selective, ATP-competitive pan-Akt inhibitor that inhibits Akt1 (IC50:5 nM), Akt2 (IC50:18 nM), and Akt3 (IC50:8 nM). Ipatasertib (GDC-0068) can lead to p53-independent PUMA activation by inhibiting Akt, thereby activating FoxO3a and NF-κB simultaneously, directly binding to the PUMA promoter, upregulating PUMA transcription and Bax-mediated intrinsic mitochondrial apoptosis.

Antitumor agent-83 acts as a BAX pro-apoptotic protein activator, significantly inhibiting tumor cell proliferation and mediating cell apoptosis through BAX's conformational activation. It also impedes the A549 cell cycle, demonstrating robust metabolic stability and an in vitro CYPs spectrum.

Antiproliferative agent-23, a microtubule-destabilizing agent (MDA), disrupts the tubulin-microtubule system, leading to apoptosis through a mitochondrion-dependent pathway. This involves downregulation of Bcl-2 protein, upregulation of Bax and Cyt c proteins, and activation of the caspase cascade. Additionally, it induces reactive oxygen species (ROS)-mediated endoplasmic reticulum stress in A549/CDDP cells (cisplatin-resistant cancer cell line) through the PERK/ATF4/CHOP signaling pathway, demonstrating anti-tumor activity [1].

Humanin, a 24-amino acid anti-apoptotic peptide and Bax inhibitor, prevents Bax translocation from the cytosol to mitochondria and obstructs its activation. This mitochondria-associated peptide has neuroprotective properties against Alzheimer's Disease (AD)-related neurotoxicity and enhances insulin sensitivity in animals, linking it to aging processes [1] [2]. An analogue named HNG, with serine at position 14 substituted for glycine, has been developed [2].

BH3 hydrochloride, a peptide that crosses the blood-brain barrier, induces apoptosis either through direct activation of the pro-apoptotic proteins Bax/Bak or by inhibiting anti-apoptotic Bcl-2 proteins (Bcl-2, Bcl-XL, Bcl-w, Mcl-1, and A-1) through their BH3 domain [1][2].

Bid BH3 (80-99) is a biologically active peptide and a pro-apoptotic member of the 'BH3-only' (BOPS) subset within the BCL-2 protein family, crucial in apoptosis regulation. It interacts with Bcl-2, Bax, and Bak to initiate their activation or inactivation, inducing cell death. Bid translocates from the cytosol to the mitochondrial membrane as part of its mechanism. Pyroglutamyl (pGlu) peptides, which can arise from Glutamine (Q) or Glutamic acid (E) at the N-terminus, have a hydrophobic γ-lactam ring that enhances stability and provides resistance to gastrointestinal proteases. These peptides are recognized variants in peptide analyses, including HPLC purity assessments.

BAI1 hydrochloride is a selective inhibitor of the apoptosis factor BAX, functioning through an allosteric mechanism. By binding to BAX, it allosterically inhibits its activation, showcasing potential applications in the research of diseases mediated by BAX-dependent cell death [1].

Phytosphingosine is a phospholipid with anticancer properties. In cancer cells, Phytosphingosine induces cell apoptosis through activation of caspase 8 and translocation of Bax.

Serratenediol demonstrates strong inhibitory effects on the Epstein-Barr virus early antigen (EBV-EA) activation without showing any cytotoxicity, its effects being stronger than that of a representative control, oleanolic acid. Serratenediol can promote