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MedChemExpressModel NVP-ADW742 - 475488-23-4

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NVP-ADW742 (ADW742) is an orally active, selective IGF-1R tyrosine kinase inhibitor with an IC50 of 0.17 μM. NVP-ADW742 inhibits insulin receptor (InsR) with an IC50 of 2.8 μM. NVP-ADW742 induces pleiotropic antiproliferative/proapoptotic biologic sequelae in tumor cells[1][2].
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NVP-ADW742

MCE China:NVP-ADW742

Brand:MedChemExpress (MCE)

Cat. No.HY-10252

CAS:475488-23-4

Synonyms:ADW742; GSK 552602A; ADW

Purity:99.54%

Storage:Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year

Shipping:Room temperature in continental US; may vary elsewhere.

Description:NVP-ADW742 (ADW742) is an orally active, selective IGF-1R tyrosine kinase inhibitor with an IC50 of 0.17 μM. NVP-ADW742 inhibits insulin receptor (InsR) with an IC50 of 2.8 μM. NVP-ADW742 induces pleiotropic antiproliferative/proapoptotic biologic sequelae in tumor cells.

In Vitro:NVP-ADW742 (ADW742; 0.1-10 μM; 72 hours) dose-dependently inhibits serum-induced cell growth in all cell lines[1]. NVP-ADW742 (0.1-9 μM; 20 min) blocks IGF-1-induced phosphorylation of IGF-1R and its known downstream target Akt at submicromolar concentrations[1]. NVP-ADW742 has much higher IC50 values for other kinases (IC50>10 μM for HER2, PDGFR, VEGFR-2, or Bcr-Abl p210; and IC50>5 μM for c-Kit)[1].

In Vivo:NVP-ADW742 (ADW742; 10 mg/kg for IP or 50 mg/kg for orally; twice daily for 19 days) significantly suppresses tumor growth and prolongs the survival of mice[1].

IC50 & Target:IC50: 0.17 μM (IGF-1R) and 2.8 μM (InsR)[1] Cellular Effect Cell Line Type Value Description References

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References:

[1]. Mitsiades CS, et al. Inhibition of the insulin-like growth factor receptor-1 tyrosine kinase activity as a therapeutic strategy for multiple myeloma, other hematologic malignancies, and solid tumors. Cancer Cell. 2004 Mar;5(3):221-30.  [Content Brief]

[2]. Warshamana-Greene GS, et al. The insulin-like growth factor-I (IGF-I) receptor kinase inhibitor NVP-ADW742, in combination with STI571, delineates a spectrum of dependence of small cell lung cancer on IGF-I and stem cell factor signaling. Mol Cancer Ther. 2004 May;3(5):527-35.  [Content Brief]

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