23133-56-4
Chemical Structure
Physalin B
- CAS No.: 23133-56-4
- Formula:C28H30O9
- Molecular Weight:510.53
InChIKey: HVTFEHJSUSPQBK-DNJDGUCCSA-N
SMILES: C[C@@]([C@H](OC1=O)C2)(OC3=O)[C@](O[C@@]45C6=O)([C@@]3(CC[C@@]7([H])[C@@]4([H])CC=C(CC=C8)[C@@]7(C8=O)C)O)[C@]6([H])[C@]2([C@@]1([H])CO5)C
Biological Activity: Physalin B is an orally active anti-inflammatory and anticancer agent. Physalin B can be isolated from Physalis alkekengi L. var. Franchetii. Physalin B inhibits the activation of the NF-κB, NLRP3 inflammasome, STAT3, PI3K/Akt and Hedgehog signaling pathways, regulates the phosphorylation levels of GSK-3β, p38 MAPK, ERK1/2 and JNK, and promotes the nuclear translocation of NRF2. Physalin B reduces the levels of pro-inflammatory cytokines and factors, induces mitochondrial reactive oxygen species (mito-ROS) production, Apoptosis, G2/M cell cycle arrest and incomplete Autophagy, alters cytoskeleton structure and alleviates oxidative stress. Physalin B reduces cancer cell viability, ameliorates liver and lung tissue damage and alleviates liver fibrosis. Physalin B can be used in research related to ulcerative colitis, breast cancer, acute lung injury, colon cancer, non-alcoholic steatohepatitis, liver fibrosis, lung cancer, pancreatic cancer, lymphoma, ovarian cancer, sarcoma and leukemia[1][2][3][4][5][6][7].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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Physalin B | 97.20% | Physalin B is an orally active anti-inflammatory and anticancer agent. Physalin B can be isolated from Physalis alkekengi L. var. Franchetii. Physalin B inhibits the activation of the NF-κB, NLRP3 inflammasome, STAT3, PI3K/Akt and Hedgehog signaling pathways, regulates the phosphorylation levels of GSK-3β, p38 MAPK, ERK1/2 and JNK, and promotes the nuclear translocation of NRF2. Physalin B reduces the levels of pro-inflammatory cytokines and factors, induces mitochondrial reactive oxygen species (mito-ROS) production, Apoptosis, G2/M cell cycle arrest and incomplete Autophagy, alters cytoskeleton structure and alleviates oxidative stress. Physalin B reduces cancer cell viability, ameliorates liver and lung tissue damage and alleviates liver fibrosis. Physalin B can be used in research related to ulcerative colitis, breast cancer, acute lung injury, colon cancer, non-alcoholic steatohepatitis, liver fibrosis, lung cancer, pancreatic cancer, lymphoma, ovarian cancer, sarcoma and leukemia. | ||||||||||||||||||||
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References
- [1]. Zhang Q, et al. Anti-colitic effects of Physalin B on dextran sodium sulfate-induced BALB/c mice by suppressing multiple inflammatory signaling pathways. Journal of ethnopharmacology. 2020 Sep 15;259:112956. [Content Brief]
- [2]. Wang A, et al. Physalin B induces cell cycle arrest and triggers apoptosis in breast cancer cells through modulating p53-dependent apoptotic pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2018 May;101:334-341. [Content Brief]
- [3]. Zhong R, et al. Physalin B ameliorates inflammatory responses in lipopolysaccharide-induced acute lung injury mice by inhibiting NF-κB and NLRP3 via the activation of the PI3K/Akt pathway. Journal of ethnopharmacology. 2022 Feb 10;284:114777. [Content Brief]
- [4]. Ma YM, et al. Physalin B not only inhibits the ubiquitin-proteasome pathway but also induces incomplete autophagic response in human colon cancer cells in vitro. Acta pharmacologica Sinica. 2015 Apr;36(4):517-27. [Content Brief]
- [5]. Zhang MH, et al. Physalin B ameliorates nonalcoholic steatohepatitis by stimulating autophagy and NRF2 activation mediated improvement in oxidative stress. Free radical biology & medicine. 2021 Feb 20;164:1-12. [Content Brief]
- [6]. Vandenberghe I, et al. Physalin B, a novel inhibitor of the ubiquitin-proteasome pathway, triggers NOXA-associated apoptosis. Biochemical pharmacology. 2008 Aug 15;76(4):453-62. [Content Brief]
- [7]. Zhu X, et al. Physalin B attenuates liver fibrosis via suppressing LAP2α-HDAC1-mediated deacetylation of the transcription factor GLI1 and hepatic stellate cell activation. Br J Pharmacol. 2021 Sep;178(17):3428-3447. [Content Brief]
