Idelalisib

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

Idelalisib (CAL-101, GS-1101) 是一种有效的选择性 PI3K p110δ 抑制剂，IC50 为 2.5 nM。

Idelalisib (CAL-101, GS-1101) is a potent, selective inhibitor of PI3K p110δ with IC50 of 2.5 nM, 40- to 300-fold selectivity over other class I PI3Ks (p110α/βγ, IC50=820/565/89nM), and 400- to 4000-fold over C2β, hVPS34, DNA-PK, and mTOR; blocks Fc?RI p110δ-mediated CD63 expression in basophils with an EC50 of 8 nM; blocks constitutive PI3K signaling, resulting in decreased phosphorylation of Akt and other downstream effectors, an increase in PARP and caspase cleavage and an induction of apoptosis in multiple B-cell malignancies.Blood Cancer Approved(In Vitro):Idelalisib (CAL-101; GS-1101) is a highly selective and potent p110δ inhibitor (EC50=8 nM). Greater selectivity (400- to 4000-fold) is seen against related kinases C2β, hVPS34, DNA-PK, and mTOR, whereas no activity is observed against a panel of 402 diverse kinases at 10 μM. CAL-101 reduces PDGF-induced pAkt by only 25% at 10 μM. Idelalisib (CAL-101) inhibits LPA-induced pAkt with an EC50 of 1.9 μM. Idelalisib (CAL-101) blocks Fc?RI p110δ-mediated CD63 expression with an EC50 of 8 nM, whereas formyl-methionyl-leucyl-phenylalanine activation of p110γ is inhibited with an EC50 of 3 μM. Thus, in cell-based assays, CAL-101 has 240- to 2500-fold selectivity for p110δ over the other class I PI3K isoforms. CAL-101Idelalisib (CAL-101)-induced apoptosis of chronic lymphocytic leukemia (CLL) cells is significant compare with vehicle treatment alone (P<0.001). Idelalisib (CAL-101) induces selective cytotoxicity in CLL cells independent of IgVH mutational status or interphase cytogenetics.(In Vivo):A significant reduction is observed in the CD11b+Ly6G+ neutrophils from brain homogenates of bothp110δD910A/D910A mice and Idelalisib (CAL-101) (40 mg/kg, i.v.) post-treated mice.

Idelalisib (CAL-101; GS-1101) is a highly selective and potent p110δ inhibitor (EC50=8 nM). Greater selectivity (400- to 4000-fold) is seen against related kinases C2β, hVPS34, DNA-PK, and mTOR, whereas no activity is observed against a panel of 402 diverse kinases at 10 μM. CAL-101 reduces PDGF-induced pAkt by only 25% at 10 μM. Idelalisib (CAL-101) inhibits LPA-induced pAkt with an EC50 of 1.9 μM. Idelalisib (CAL-101) blocks Fc?RI p110δ-mediated CD63 expression with an EC50 of 8 nM, whereas formyl-methionyl-leucyl-phenylalanine activation of p110γ is inhibited with an EC50 of 3 μM. Thus, in cell-based assays, CAL-101 has 240- to 2500-fold selectivity for p110δ over the other class I PI3K isoforms. CAL-101Idelalisib (CAL-101)-induced apoptosis of chronic lymphocytic leukemia (CLL) cells is significant compare with vehicle treatment alone (P<0.001). Idelalisib (CAL-101) induces selective cytotoxicity in CLL cells independent of IgVH mutational status or interphase cytogenetics.

A significant reduction is observed in the CD11b+Ly6G+ neutrophils from brain homogenates of bothp110δD910A/D910A mice and Idelalisib (CAL-101) (40 mg/kg, i.v.) post-treated mice.

CAL-101 | GS-1101 | GS1101 | GS1101

PI3K/Akt/mTOR signaling

PI3K

hVps34|p110α|p110β|p110γ|p110δ

Cancer

Blood cancer

870281-82-6

415.423

C22H18FN7O

>98% (HPLC)

DMSO: ≥ 59.7 mg/mL

O=C1N(C2=CC=CC=C2)C([C@@H](NC3=C4N=CNC4=NC=N3)CC)=NC5=C1C(F)=CC=C5

4(3H)-Quinazolinone, 5-fluoro-3-phenyl-2-[(1S)-1-(9H-purin-6-ylamino)propyl]-

(-20℃)

With Ice Pack

≥ 2 years