Bad
BAD is a pro-apoptotic BH3-only Bcl-2 family protein that promotes apoptosis by binding Bcl-xL and Bcl-2, displacing BAX, and reversing death-repressor activity[1]. Mechanistically, survival-factor signaling phosphorylates BAD, causing 14-3-3 binding rather than Bcl-xL binding, while Akt phosphorylation blocks BAD-induced neuronal death[2][3]. Therefore, BAD links growth-factor survival pathways to the intrinsic mitochondrial apoptosis machinery, where Bcl-2 family interactions control apoptotic commitment[3][4]. In disease-relevant metabolic models, BAD resides in a glucokinase-containing mitochondrial complex that integrates glycolysis and apoptosis, and BAD deficiency or non-phosphorylatable BAD mutants impair glucose homeostasis[5]. In pancreatic β-cells, BAD supports glucose-stimulated insulin secretion and β-cell survival, giving BAD practical value in diabetes-related apoptosis and metabolism studies[6]. Compared with activator isoforms such as BID, BIM, and PUMA, BAD functions mainly as a sensitizer that neutralizes anti-apoptotic Bcl-2 proteins rather than directly activating BAX-BAK[4]. For experimental applications, phospho-BAD BH3 helix mimetics activate glucokinase through a mechanism distinct from classical allosteric activators[7].
References:
- [1]. Yang E, et al. Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death. Cell. 1995 Jan 27;80(2):285-91. [Content Brief]
- [2]. Zha J, et al. Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L). Cell. 1996 Nov 15;87(4):619-28. [Content Brief]
- [3]. Datta SR, et al. Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery. Cell. 1997 Oct 17;91(2):231-41. [Content Brief]
- [4]. Hongay CF, et al. Antisense transcription controls cell fate in Saccharomyces cerevisiae. Cell. 2006 Nov 17;127(4):735-45. [Content Brief]
- [5]. Danial NN, et al. BAD and glucokinase reside in a mitochondrial complex that integrates glycolysis and apoptosis. Nature. 2003 Aug 21;424(6951):952-6. [Content Brief]
- [6]. Danial NN, et al. Dual role of proapoptotic BAD in insulin secretion and beta cell survival. Nat Med. 2008 Feb;14(2):144-53. [Content Brief]
- [7]. Szlyk B, et al. A phospho-BAD BH3 helix activates glucokinase by a mechanism distinct from that of allosteric activators. Nat Struct Mol Biol. 2014 Jan;21(1):36-42. [Content Brief]
All Product Categories
-
Bad Related Products (10)
Related Products (10)
-
ML281
0 ImagesML281 is a highly selective inhibitor of serine/threonine kinase 33 (STK33) with an IC50 value of 14 nM. ML281 shows 700-fold selectivity over PKA and 550-fold over AurB. ML281 exerts core mechanism by inhibiting STK33: in small cell lung cancer, ML281 downregulates RPS6/BAD signaling phosphorylation, induces apoptosis, and suppresses proliferation, invasion. ML281 reduces STK33-mediated 4-hydroxyphenylpyruvate dioxygenase (HPD) phosphorylation in tyrosinemia . ML281 is suitable for research on STK33 function, KRAS mutation-related cancers (pancreatic cancer, colon cancer, lung adenocarcinoma, etc.), small cell lung cancer, and tyrosinemia-related damage
-
Caudatin
0 ImagesCaudatin is an orally active and brain-penetrant C-21 steroidal found in Cynanchum bungei decne with a variety of biological activities. Caudatin can inhibit cell proliferation, migration, invasion, cause cell phase arrest, induce apoptosis, autophagy, ROS prodution and loss of mitochondrial membrane potential. Caudatin activates PARP, caspase-3, -7, -9, upregulates pro-apoptotic Bad and Bax and downregulates anti-apoptotic Bcl-2 and Bcl-XL. Caudatin suppresses VEGF, FAK phosphorylation, upregulates p21, p27, DR5 protein expression, activates the p38 MAPK, JNK and PPARα/TFEB-mediated autophagy-lysosomal signaling pathways. Caudatin can be used for the research of cancer, inflammation and neurological disease, such as glioma and Alzheimer's disease.
-
Desethylamiodarone hydrochloride
0 ImagesSynonyms: N-Desethylamiodarone hydrochloride; LB 33020 hydrochlorideDesethylamiodarone hydrochloride (N-Desethylamiodarone hydrochloride; LB 33020 hydrochloride) is the major active metabolite of Amiodarone (HY-14187) generated via CYP3A4 metabolism. Desethylamiodarone hydrochloride downregulates p‑Akt, p‑Bad and Bcl‑2, upregulates Bax, promotes mitochondrial release of cytochrome c, activates caspase‑3 and cleaves PARP‑1, thereby inducing cell cycle arrest and apoptosis. Desethylamiodarone hydrochloride can be used in cervical cancer-related research.
-
Desethylamiodarone
0 ImagesCat. No.: HY-122423CAS No.: 83409-32-9Synonyms: N-Desethylamiodarone; LB 33020Desethylamiodarone (N-Desethylamiodarone; LB 33020) is the major active metabolite of Amiodarone (HY-14187) generated via CYP3A4 metabolism. Desethylamiodarone downregulates p‑Akt, p‑Bad and Bcl‑2, upregulates Bax, promotes mitochondrial release of cytochrome c, activates caspase‑3 and cleaves PARP‑1, thereby inducing cell cycle arrest and apoptosis. Desethylamiodarone can be used in cervical cancer-related research.
-
XAN-5
0 ImagesCat. No.: HY-181599XAN-5 is a mitochondrial DNA G-quadruplex (mtG4) ligand with a Kd of 3.8 μM. XAN-5 selectively binds and stabilizes mtG4 structures, disrupting mitochondrial gene transcription and DNA replication. XAN-5 triggers mitochondrial dysfunction, ROS overproduction, G0 phase arrest and caspase-dependent apoptosis. XAN-5 inhibits autophagy and induces immunogenic cell death. XAN-5 inhibits tumor growth in a mouse liver cancer model while enhancing tumor-infiltrating CD4+ and CD8+ T cells. XAN-5 targets two cancer resistance mechanisms simultaneously. XAN-5 can be used for the research of liver cancer.
-
Desethylamiodarone-d4 hydrochloride
0 ImagesCat. No.: HY-130353SCAS No.: 1189960-80-2Synonyms: N-Desethylamiodarone-d4 hydrochloride; LB 33020-d4 hydrochlorideDesethylamiodarone-d4 hydrochloride (N-Desethylamiodarone-d4 hydrochloride; LB 33020-d4 hydrochloride) is the deuterated-labeled Desethylamiodarone hydrochloride (HY-130353). Desethylamiodarone hydrochloride (N-Desethylamiodarone hydrochloride; LB 33020 hydrochloride) is the major active metabolite of Amiodarone (HY-14187) generated via CYP3A4 metabolism. Desethylamiodarone hydrochloride downregulates p‑Akt, p‑Bad and Bcl‑2, upregulates Bax, promotes mitochondrial release of cytochrome c, activates caspase‑3 and cleaves PARP‑1, thereby inducing cell cycle arrest and apoptosis. Desethylamiodarone hydrochloride can be used in cervical cancer-related research.
-
Desethylamiodarone hydrochloride (Standard)
0 ImagesCat. No.: HY-130353RCAS No.: 96027-74-6Synonyms: N-Desethylamiodarone hydrochloride (Standard); LB 33020 hydrochloride (Standard)Desethylamiodarone hydrochloride (Standard) (N-Desethylamiodarone hydrochloride (Standard); LB 33020 hydrochloride (Standard)) is the analytical standard of Desethylamiodarone hydrochloride (HY-130353). This product is intended for research and analytical applications. Desethylamiodarone hydrochloride (N-Desethylamiodarone hydrochloride; LB 33020 hydrochloride) is the major active metabolite of Amiodarone (HY-14187) generated via CYP3A4 metabolism. Desethylamiodarone hydrochloride downregulates p‑Akt, p‑Bad and Bcl‑2, upregulates Bax, promotes mitochondrial release of cytochrome c, activates caspase‑3 and cleaves PARP‑1, thereby inducing cell cycle arrest and apoptosis. Desethylamiodarone hydrochloride can be used in cervical cancer-related research.
-
Tubulin polymerization-IN-85
0 ImagesCat. No.: HY-180190Tubulin polymerization-IN-85 (Compound C21) is a tubulin polymerization inhibitor (IC50 = 1.59 μM) targeting the colchicine binding site. Tubulin polymerization-IN-85 can cause cancer cells G2/M phase arrest and induce apoptosis. Tubulin polymerization-IN-85 downregulates the expression of Bcl-2, Bcl-xl, Mcl-1, Cyclin B1, cdc25, cdc2 protein and upregulates P53, P21, Bad and Bax levels. Tubulin polymerization-IN-85 can be used for the research of cancer, such as cervical cancer.
-
FLC-8
0 ImagesCat. No.: HY-182937CAS No.: 3100242-36-9FLC-8 is an orally active FLT3 inhibitor with IC50 values of 10.2 nM, 11.6 nM and 24.10 nM against human FLT3-WT, FLT3-G697R and FLT3-N676D, respectively. FLC-8 inhibits FLT3 autophosphorylation and downstream STAT5, AKT and ERK signaling pathways, and induces apoptosis in acute myeloid leukemia (AML) cells. FLC-8 exhibits potent antitumor activity in the MV4-11 xenograft model. FLC-8 can be used for the research of acute myeloid leukemia.
