MK-1775(AZD-1775,Adavosertib)

Cas No.:	955365-80-7
Chemical Name:	Adavosertib
Synonyms:	2-Allyl-1-(6-(2-hydroxypropan-2-yl)pyridin-2-yl)-6-((4-(4-methylpiperazin-1-yl)phenyl)amino)-1H-pyrazolo[3,4-d]pyrimidin-3(2H)-one;MK-1775;1-[6-(2-hydroxypropan-2-yl)pyridin-2-yl]-6-[4-(4-methylpiperazin-1-yl)anilino]-2-prop-2-enylpyrazolo[3,4-d]pyrimidin-3-one;2-ALLYL-1-(6-(2-HYDROXYPROPAN-2-YL)PYRIDIN-2-YL)-6-(4-(4-METHYLPIPERAZIN-1-YL)PHENYLAMINO)-1H-PYRAZOLO[3,4-D]PYRIMIDIN-...;2-Allyl-1-(6-(2-hydroxypropan-2-yl)pyridin-2-yl)-6-(4-(4-methylpiperazin-1-yl)phenylamino)-1H-pyrazolo[3,4-d]pyrimidin-3(2H)-one;AZD-1775;MK 1775;MK-1775 (MK 1775, MK1775);MK-1775, AZD1775;AZD1775;2-allyl-1-(6-(2-hydroxypropan-2-yl)pyridin-2-yl)-6-(4-(4-methylpiperazin-1-yl)phenylamino)-1,2-dihydropyrazolo[3,4-d]pyrimidin-3-one;Adavosertib;MK1775;AZD 1775;K2T6HJX3I3;1-[6-(2-
SMILES:	C=CCN1N(C2=NC(=CC=C2)C(C)(C)O)C3C(=CN=C(NC4=CC=C(C=C4)N5CCN(C)CC5)N=3)C1=O
Formula:	C27H32N8O2
M.Wt:	500.5954
Sotrage:	2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO

Description:	Adavosertib (AZD-1775; MK-1775) is a potent Wee1 inhibitor with an IC50 of 5.2 nM.
In Vivo:	In vivo, Adavosertib (MK-1775) potentiates the anti-tumor efficacy of 5-FU or its prodrug, capecitabine, at tolerable doses[1]. Adavosertib (MK-1775) (60 mg/kg twice daily, p.o.) enhances H1299 xenograft tumor response to fractionated radiotherapy[2]. Adavosertib (MK-1775) (30 mg/kg. p.o.) regresses tumor growth in PANC198, PANC215 and PANC185 as compared to GEM treated mice[3].
In Vitro:	Adavosertib (MK-1775) enhances the cytotoxic effects of 5-FU in p53-deficient human colon cancer cells. Adavosertib (MK-1775) inhibits CDC2 Y15 phosphorylation in cells, abrogates DNA damaged checkpoints induced by 5-FU treatment, and causes premature entry of mitosis determined by induction of Histone H3 phosphorylation[1]. Adavosertib (MK-1775) abrogates the radiation-induced G2 block in p53-defective cells but not in p53 wild-type lines[2]. The combination of gemcitabine with Adavosertib (MK-1775) produces robust anti-tumor activity and remarkably enhances tumor regression response (4.01 fold) compared to gemcitabine treatment in p53-deficient tumors[3].