Tanespimycin

Tanespimycin (17-AAG) is a potent HSP90 inhibitor with an IC50 of 5 nM, having a 100-fold higher binding affinity for tumour cell derived HSP90 than normal cell derived HSP90[1][5]. Tanespimycin depletes cellular STK38/NDR1 and reduces STK38 kinase activity. Tanespimycin also downregulates the stk38 gene expression[3].

75747-14-7

17-AAG; NSC 330507; CP 127374

12352005

H302, H315, H319, H335

Antibiotic; Apoptosis; Autophagy; Bacterial; HSP; Mitophagy

Reference compound

Anti-infection; Apoptosis; Autophagy; Cell Cycle/DNA Damage; Metabolic Enzyme/Protease

Cancer-Kinase/protease

Cancer; Infection

https://www.medchemexpress.com/17-AAG.html

99.01

DMSO : 50 mg/mL (ultrasonic)

O=C(C(NC(/C(C)=C/C=C\[C@H](OC)[C@H](/C(C)=C/[C@@H]([C@H]([C@H](C[C@@H](C1)C)OC)O)C)OC(N)=O)=O)=CC2=O)C1=C2NCC=C

C31H43N3O8

585.69

H302, H315, H319, H335

[1]Solit DB, et al. 17-Allylamino-17-demethoxygeldanamycin induces the degradation of androgen receptor and HER-2/neu and inhibits the growth of prostate cancer xenografts.Clin Cancer Res, 2002, 8 (5), 986-993.|[2]Raja, Srikumar M., et al. 17-AAG induces enhanced ubiquitinylation and lysosomal pathway-dependent ErbB2 degradation and cytotoxicity in ErbB2-overexpressing breast cancer cells. Cancer Biology & Therapy (2008), 7 (10), 163|[3]Zhang J, et al. The heat shock protein 90 inhibitor 17-AAG suppresses growth and induces apoptosis in human cholangiocarcinoma cells.Clin Exp Med. 2012 Sep 7.|[4]Newman B, et al. HSP90 Inhibitor 17-AAG Selectively Eradicates Lymphoma Stem Cells.Cancer Res. 2012 Sep 1;72 (17) :4551-61. Epub 2012 Jun 29.|[5]Kamal A, et al. A high-affinity conformation of Hsp90 confers tumour selectivity on Hsp90 inhibitors. Nature. 2003 Sep 25;425 (6956) :407-10.|[6]Enomoto A, et al. The HSP90 inhibitor 17-allylamino-17-demethoxygeldanamycin modulates radiosensitivity by downregulating serine/threonine kinase 38 via Sp1 inhibition. Eur J Cancer. 2013 Nov;49 (16) :3547-58.

Room Temperature

4°C (Powder, protect from light)

Reference compound1

Phase 3