| Identification | Back Directory | [Name]
PKI-402 | [CAS]
1173204-81-3 | [Synonyms]
CS-167
PKI-402
PKI-402;PKI402
PKI-402 USP/EP/BP
1-(4-(3-Ethyl-7-morpholino-3H-[1,2,3]triazolo[4,5-d]pyrimidin-5-yl)phenyl)-3-(4-(4-methylpiper
1-(4-(3-ethyl-7-morpholino-3H-[1,2,3]triazolo[4,5-d]pyrimidin-5-yl)phenyl)-3-(4-(1-methylpiperazine-4-carbonyl)phenyl)urea
1-(4-(3-ethyl-7-morpholino-3H-[1,2,3]triazolo[4,5-d]pyrimidin-5-yl)phenyl)-3-(4-(4-methylpiperazine-1-carbonyl)phenyl)urea
1-[4-[3-Ethyl-7-(morpholin-4-yl)-3H-[1,2,3]triazolo[4,5-d]pyrimidin-5-yl]phenyl]-3-[4-[(4-methylpiperazin-1-yl)carbonyl]phenyl]urea
Urea, N-[4-[3-ethyl-7-(4-morpholinyl)-3H-1,2,3-triazolo[4,5-d]pyrimidin-5-yl]phenyl]-N'-[4-[(4-methyl-1-piperazinyl)carbonyl]phenyl]- | [Molecular Formula]
C29H34N10O3 | [MDL Number]
MFCD18251484 | [MOL File]
1173204-81-3.mol | [Molecular Weight]
570.645 |
| Chemical Properties | Back Directory | [Boiling point ]
670.6±55.0 °C(Predicted) | [density ]
1.43 | [storage temp. ]
Store at -20°C | [solubility ]
insoluble in EtOH; insoluble in H2O; ≥14.28 mg/mL in DMSO | [form ]
solid | [pka]
13.80±0.70(Predicted) | [color ]
White to off-white |
| Hazard Information | Back Directory | [Uses]
A selective, reversible and ATP-competitive Class I PI3K inhibitor. PI3Kα, IC50=1 nM; PI3Kβ, IC50=7 nM; PI3Kγ, IC50=16 nM; PI3Kδ, IC50=14 nM. | [Biological Activity]
pki-402 is a selective, equipotent and atp-competitive class i pi3k inhibitor (ic50= 1 nm, 7 nm, 16 nm and 14 nm for pi3kα, pi3kβ, pi3kγ and pi3kδ, respectively.)pi3k (phosphatidylinositol-4,5-bisphosphate 3-kinase) is a family of enzymes involved in cellular functions such as cell growth, proliferation, differentiation, motility, survival and intracellular trafficking, which in turn are involved in cancer. it plays a key role in pi3k/akt/mtor pathway.in multiple human cancer cell lines (e.g. breast, brain, pancreas and nscl), pki-402 inhibited growth of cancer cells, and attenuated phosphorylation of effector of pi3k and mtor. in mda-mb-361, 30 nm pki-402 caused cleaved of the apoptosis marker—parp.in mda-mb-361 mouse tumor xenograft models, administration of 100 mg/kg of pki-402 daily for 5 days decreased the initial tumor volume from 260 mm3 to 129 mm3 and inhibited tumor regrowth for 70 days, single dose of pki-402 blocked phosphorylation of akt and led to cleaved parp.1. mallon r, hollander i, feldberg l et al. antitumor efficacy profile of pki-402, a dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor. mol cancer ther. 2010 apr;9(4):976-84. | [in vivo]
PKI-402 displays antitumor activity (i.v. route) in breast [MDA-MB-361: Her2+ and PIK3CA (E545K)], glioma (U87MG and PTEN), and NSCLC (A549; K-Ras and STK11) xenograft models. PKI-402 causes regression in the MDA-MB-361 xenograft model. PKI-402 effect is most pronounced at 100 mg/kg (daily for 5 days, one round), which reduces initial tumor volume and prevents tumor re-growth for 70 days. In MDA-MB-361 tumor tissue, PKI-402 at 100 mg/kg (single dose) fully suppresses p-Akt at both the T308 and the S473 sites at 8 hours and induces cleaved PARP. At 24 hours, p-Akt suppression is still evident, as is cleaved PARP[1]. | [target]
PI3Kα | [IC 50]
PI3Kα: 2 nM (IC50); PI3Kα-H1047R: 3 nM (IC50); PI3Kα-E545K: 3 nM (IC50); PI3Kβ: 7 nM (IC50); PI3Kδ: 14 nM (IC50); PI3Kγ: 16 nM (IC50); mTOR: 3 nM (IC50) | [storage]
Store at -20°C |
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