pilaralisib Property

Melting point:

216-220oC

Density 

1.458±0.06 g/cm3(Predicted)

storage temp. 

Refrigerator

solubility 

DMSO (Slightly)

pka

6.33±0.30(Predicted)

form 

Solid

color 

Light Yellow to Yellow

Hazard and Precautionary Statements (GHS)

Symbol(GHS)

Signal word

Danger

Hazard statements

H302Harmful if swallowed

H372Causes damage to organs through prolonged or repeated exposure

Precautionary statements

P260Do not breathe dust/fume/gas/mist/vapours/spray.

P264Wash hands thoroughly after handling.

P264Wash skin thouroughly after handling.

P270Do not eat, drink or smoke when using this product.

P301+P312IF SWALLOWED: call a POISON CENTER or doctor/physician IF you feel unwell.

P314Get medical advice/attention if you feel unwell.

P330Rinse mouth.

P501Dispose of contents/container to..…

pilaralisib Chemical Properties,Usage,Production

Uses

Pilaralisib is a pan-PI3K inhibitor used in the treatment of patients with chronic lymphocytic leukemia or relapsed or refractory lymphoma.

Enzyme inhibitor

This selective, reversible, and ATP-competitive Class I PI3K inhibitor (FW = 541.02 g/mol; CAS 934526-89-3; Solubility: 100 mg/mL DMSO, when warmed; < 1 mg/mL H2O), also known as XL147, SAR245408, and N-(3- {[(3-{[2-chloro-5-(methoxy)phenyl]-amino}quinoxalin-2- yl)amino]sulfonyl}phenyl)-2-methylalaninamide, targets PI3Kα (IC50 = 39 nM, PI3Kδ (IC50 = 36 nM), and PI3Kγ (IC50 = 23 nM), but only weakly for PI3Kβ. Pilaralisib is active against human breast cancer cell lines with constitutive PI3K activation. PI3K inhibitors reduce AKT activity and relieves suppression of receptor tyrosine kinase expression and activity. XL147 shows dose-dependent inhibition of cell growth and levels of pAKT and pS6, signal transducers in the PI3K/AKT/TOR pathway. In HER2- overexpressing cells, pilaralisib inhibition of PI3K is attended by upregulation of expression and phosphorylation of multiple receptor tyrosine kinases, including HER3. Knockdown of FoxO1 and FoxO3a transcription factors suppressed the induction of HER3, InsR, IGF1R, and FGFR2 mRNAs upon inhibition of PI3K. In HER2(+) cells, knockdown of HER3 with siRNA or cotreatment with the HER2 inhibitors trastuzumab or lapatinib enhance XL147-induced cell death and inhibition of pAKT and pS6. When tested separately, trastuzumab and lapatinib synergized with XL147 for inhibition of pAKT and growth of established BT474 xenografts. Compared with XL147 alone, the combination exhibited a superior antitumor effect against trastuzumab-resistant tumor xenografts.