Tanespimycin CAS# 75747-14-7

Tanespimycin, Promotion Season Now in Store and Free Sample for Testing with Factory Price

• Chemical Name: Tanespimycin
• CAS No.: 75747-14-7
• Molecular Formula: C31H43N3O8
• Molecular weight: 585.69
• Appearance: Dark purple solid
• Sample: Available

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Description of Tanespimycin

Tanespimycin (17-N-allylamino-17-demethoxygeldanamycin, 17-AAG) is a derivative of the antibiotic geldanamycin that is being studied in the treatment of cancer, specific young patients with certain types of leukemia or solid tumors, especially kidney tumors.

It works by inhibiting Hsp90, which is expressed in those tumors.

It belongs to the family of drugs called antitumor antibiotics.

Basic Info of Tanespimycin

Basic Info
Numbering system
Properties
Safety Info
Basic Info

Numbering system

Properties

Safety Info

What is Tanespimycin?

With the progress of science and technology and the development of society, chemical products have invariably permeated our daily lives, in medicine, food, cosmetics, electronics, industry, and other areas, becoming an essential part of our lives. One such product is Tanespimycin which has developed particularly rapidly in recent years. Do you know about Tanespimycin?

The official answer: Tiratinib, molecular weight 585.69, is a stimulant.

What’s the application of Tanespimycin?

Tiratinib, molecular weight 585.69, is a stimulaTiratinib is a potent HSP90 inhibitor with an IC50 of 5 nM in a cell-free assay and binds with 100-fold higher affinity to HSP90 derived from tumor cells than to HSP90 derived from normal cells. Tiratinib induces apoptosis, necrosis, autophagy, and mitochondrial phagocytosis.

17-AAG is a potent inhibitor of heat shock protein 90 (Hsp90). 17-AAG is a less toxic analog than geldanamycin. It induces apoptosis and shows antitumor effects. 17-AAG inhibits the activity of oncogenic proteins such as N-ras, Ki-ras, c-Akt, and p185erB2.

17-AAG is an analog of geldanamycin and has a more than 100-fold higher binding affinity for Hsp90 derived from HER-2 overexpressing cancer cells (BT474, N87, SKOV3, and SKBR3) or BT474 breast cancer cells with an IC50 value of 5-6 nM. 17-AAG causes HER2, HER3, Akt, and mutant and wild-type androgen receptor (AR) degradation, resulting in RB-dependent G1 growth arrest in prostate cancer cells such as LNCaP, LAPC-4, and IC50 values of 25-45 nM for DU-145 and PC-3. 17-AAG can induce apoptosis in wild-type BCR-ABL-transformed Ba/F3 cells (IC50 of 5.2 μM), in addition to imatinib-resistant T315I and E255KBCR-transformed cells with the ability to induce apoptosis. By inducing degradation of wild-type BCR-ABL protein and mutants with IC50 values of 2.3 μM and 1.0 μM, respectively, the ABL mutant.

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