AIM-100 MedChemExpress (MCE)

Product Name	AIM-100
Synonyms	AIM100;AIM-100;AIM 100;5,6-Diphenyl-N-[[(2S)-tetrahydro-2-furanyl]methyl]furo[2,3-d]pyrimidin-4-amine;Furo[2,3-d]pyrimidin-4-amine, 5,6-diphenyl-N-[[(2S)-tetrahydro-2-furanyl]methyl]-
CAS	873305-35-2
EINECS
Chemical Formula	C23H21N3O2
Molecular Weight	371.43
inchi
Package	10 mM * 1 mL;1 mg;5 mg;10 mg;25 mg;50 mg;100 mg
Price	Email to quote
Descriptions	AIM-100 AIM-100 MedChemExpress (MCE) HY-15290 873305-35-2 99.95% Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year Room temperature in continental US Descriptions AIM-100 AIM-100 MedChemExpress (MCE) HY-15290 873305-35-2 99.95% Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year Room temperature in continental US may vary elsewhere. AIM-100 is a potent and selective Ack1 inhibitor with an IC50 of 21.58 nM. AIM-100 also inhibits Tyr267 phosphorylation. AIM-100 does not inhibits other kinases including PI3-kinase and AKT subfamily members. AIM-100 has an anticancer effect. AIM-100 (2-10 μM 48 hours) treatment not only inhibits Ack1 activation but also suppresses AKT tyrosine phosphorylation, leading to cell cycle arrest in the G1 phase. AIM-100 not only inhibits Ack1/AKT Tyr-phosphorylation but also suppressed growth of cell lines derived from pancreatic, breast, and lung tumors[1]. The Ack1 inhibitor AIM-100 not only inhibited Ack1 activity but also was able to suppress AR Tyr267 phosphorylation and its recruitment to the ataxia-telangiectasia mutated kinase (ATM) enhancer[2]. AIM-100 is able to suppress pTyr267-AR phosphorylation, binding of androgen receptor (AR) to PSA, NKX3.1, and TMPRSS2 promoters, and inhibit AR transcription activity[3]. In male nude castrated mice, AIM-100 (4 mg/kg) suppresses growth of radioresistant castration-resistant prostate cancer (CRPC) xenograft tumors by decreasing ataxia-telangiectasia mutated kinase (ATM) expression[2]. IC50: 21.58 nM (Ack1)[2] Cellular Effect Cell Line Type Value Description References \| \| \| \| \| \| \| \| \| \| [1]. Mahajan K, et al. Ack1 tyrosine kinase activation correlates with pancreatic cancer progression. Am J Pathol. 2012 Apr 180(4):1386-93. [Content Brief] [2]. Mahajan K, et al. Ack1-mediated androgen receptor phosphorylation modulates radiation resistance in castration-resistant prostate cancer. J Biol Chem. 2012 Jun 22 287(26):22112-22. [Content Brief] [3]. Mahajan K, et al. Effect of Ack1 tyrosine kinase inhibitor on ligand-independent androgen receptor activity. Prostate. 2010 Sep 1 70(12):1274-85. [Content Brief]
Last Update	2025-04-01 14:45:47

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