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Cas No.:870281-86-0

Synonyms:(S)-2-(1-aMinopropyl)-5-fluoro-3-phenylquinazolin-4(3H)-one;2-[(1S)-1-Aminopropyl]-5-fluoro-3-phenyl-4(3H)-quinazolinone;Idelalisib INT;CAL-101(N-1);CAL101(N-1);CAL 101(N-1);

MF:C17H16FN3O

NW:297.3268432

Assay: ≥99%

Packing:Export worthy packing

Material Safety Data Sheet:Available on request

Usage:CAL-101 (Idelalisib, GS-1101) is a selective p110δ inhibitor; shown to have 40- to 300-fold greater selectivity for p110δ than p110α/β/γ, and 400- to 4000-fold more selectivity to p110δ than C2β, hVPS34, DNA-PK and mTOR. Henan CoreyChem can supply the intermediate of CAL101 and also research the synthesis route of CAL101

CAL-101 (Idelalisib, GS-1101) is a selective p110δ inhibitor with IC50 of 2.5 nM; shown to have 40- to 300-fold greater selectivity for p110δ than p110α/β/γ, and 400- to 4000-fold more selectivity to p110δ than C2β, hVPS34, DNA-PK and mTOR.
IC50 value: 2.5 nM [1]
Target: p110δ
in vitro: CAL-101 is not sensitive to other PI3K class I subunits including p110α, p110β, and p110γ. CAL-101 specifically blocks Fc?R1 p110δ-mediated CD63 expression with an EC50 of 8 nM in primary basophil. CAL-101 exhibits greater activity in B-cell acute lymphoblastic leukemia (B-ALL) and chronic lymphocytic leukemia (CLL) cells compared with acute myeloid leukemia (AML) and myeloproliferative neoplasm (MPN) cells. CAL-101 produces the reduction in pAktS473, pAktT308, and the downstream target S6 in SU-DHL-5, KARPAS-422 and CCRF-SB cells with EC50 of 0.1 to 1.0 μM [1]. CAL-101 induces selective cytotoxicity in CLL cells independent of IgVH mutational status or interphase cytogenetics, primarily through a caspase-dependent mechanism. CAL-101 induces cytotoxicity preferentially to CLL cells compared with normal B cells, without producing cytotoxicity in other hematopoietic cells, compared to LY294002. CAL-101 lacks direct cytotoxic potential to T cells and nature killer (NK) cells. CAL-101 can inhibit production of inflammatory cytokines, such as IL-6, IL-10, TNF-α, and IFN-γ, and activation-induced cytokines, such as CD40L. CAL-101 also antagonizes CD40L-mediated CLL cell survival [2]. AL-101 induces an accumulation of cells in G1 and a decrease in the S-phase population in L1236 and L591 cells, which indicates CAL-101 as a novel strategy for the treatment of hodgkin lymphoma (HL) [3].

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