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Buparlisib Hydrochloride

Catalog No. T16365   CAS 1312445-63-8
Synonyms: NVP-BKM120 Hydrochloride, BKM120 Hydrochloride

Buparlisib Hydrochloride is an inhibitor of pan-class I PI3K (IC50: 52 nM/166 nM/116 nM/262 nM for p110α/p110β/p110δ/p110γ, respectively).

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Buparlisib Hydrochloride Chemical Structure
Buparlisib Hydrochloride, CAS 1312445-63-8
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Biological Description
Chemical Properties
Storage & Solubility Information
Description Buparlisib Hydrochloride is an inhibitor of pan-class I PI3K (IC50: 52 nM/166 nM/116 nM/262 nM for p110α/p110β/p110δ/p110γ, respectively).
Targets&IC50 mTOR:4.6 μM, p110α-E545K:99 nM, p110α:52 nM, p110γ:262 nM, p110δ:116 nM, p110α-H1047R:58 nM, p110β:166 nM, Vps34:2.4 μM
In vitro NVP-BKM120 shows lower potency against class III and class IV PI3K's, where 2, 5, >5, and >25 μM biochemical activity is observed for inhibition of VPS34, mTOR, DNAPK, and PI4K, respectively. Buparlisib causes multiple myeloma (MM) cell apoptosis in both dose- and time-dependent manners. Buparlisib has 50-300 nM activity for class I PI3K's, including the most common p110α mutants. Buparlisib ( ≥10 μM) induces significant apoptosis in all tested MM cell lines at 24 h (P<0.05, compares with control). Buparlisib (10 μM; 24-h) treatment is chosen in the following experiments if not stated otherwise. Buparlisib treatment causes dose-dependent growth inhibition in all tested MM cell lines. Buparlisib IC50 varies among tested MM cells. At 24 h treatment, IC50 for ARP-1, ARK, and MM.1R is between 1 and 10 μM, while IC50 for MM.1S is <1 μM, and IC50 for U266 is between 10 and 100 μM. Buparlisib treatment results in MM cell growth inhibition and apoptosis in a dose- and time-dependent manners[1][2].
In vivo Buparlisib (p.o.; 3, 10, 30, 60, and 100 mg/kg) results in a dose-dependent modulation of pAKTSer473, in A2780 xenograft tumors. Mice receiving Buparlisib (5 μM per kg per day for 15 days) treatment has significantly smaller tumor burdens as compared with control mice, which are measured as tumor volume (P<0.05) and level of circulating human kappa chain (P<0.05). Buparlisib treatment significantly prolongs the survival of tumor-bearing mice (P<0.05). Partial inhibition of pAKTSer473 is observed at 3 and 10 mg/kg, and near-complete inhibition is observed at doses of 30, 60, or 100 mg/kg, respectively. Inhibition of pAKT (normalized to total AKT) tracked well with both plasma and tumor drug exposure[1][2].
Synonyms NVP-BKM120 Hydrochloride, BKM120 Hydrochloride
Molecular Weight 446.85
Formula C18H22ClF3N6O2
CAS No. 1312445-63-8


Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

DMSO: 50 mg/mL (111.89 mM)

( < 1 mg/ml refers to the product slightly soluble or insoluble )

TargetMolReferences and Literature

1. Burger MT, et al. Identification of NVP-BKM120 as a Potent, Selective, Orally Bioavailable Class I PI3 Kinase Inhibitor for Treating Cancer. ACS Med Chem Lett. 2011 Aug 26;2(10):774-9. 2. Zheng Y, et al. Novel phosphatidylinositol 3-kinase inhibitor NVP-BKM120 induces apoptosis in myeloma cells and shows synergistic anti-myeloma activity with dexamethasone. J Mol Med (Berl). 2012 Jun;90(6):695-706.

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Buparlisib Hydrochloride 1312445-63-8 Others BKM 120 Hydrochloride NVP-BKM-120 Hydrochloride NVP-BKM 120 Hydrochloride BKM-120 Hydrochloride NVP-BKM120 Hydrochloride BKM120 Hydrochloride inhibitor inhibit