ABT-263 (Navitoclax ) is a potent and orally active Bcl-2 family protein inhibitor that binds to multiple anti-apoptotic Bcl-2 family proteins, such as Bcl-xL, Bcl-2 and Bcl-w, with a Ki of less than 1 nM.

≥98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

Navitoclax；ABT263

White solid

DMF : ≥ 100 mg/mL (102.61 mM)
DMSO : 75 mg/mL (76.95 mM; Need ultrasonic)

Bcl-xL；Bcl-2；Bcl-w

ABT-263 is structurally related to ABT-737; it is a disruptor of Bcl-2/Bcl-xL interactions with pro-apoptotic proteins. Overexpression of the prosurvival Bcl-2 family members is commonly associated with tumor maintenance, progression, and chemoresistance. ABT-263 displays the protection afforded by overexpression of Bcl-2 or Bcl-xL with EC50 values of 60 nM and 20 nM, respectively. A wide range of cellular activity is observed with ABT-263 having a 50% growth inhibition (EC50) of 110 nM against the most sensitive line (H146), whereas its activity in the least sensitive line (H82) results in an EC50 at 22 μM. All four cell lines with EC50 values of

When ABT-263 is administered at 100 mg/kg/day in the H345 xenograft model, significant antitumor efficacy is observed with 80% TGI and 20% of treated tumors indicating at least a 50% reduction in tumor volume. Oral administration of ABT-263 alone causes complete tumor regressions in xenograft models of small-cell lung cancer and acute lymphoblastic leukemia. In xenograft models of aggressive B-cell lymphoma and multiple myeloma where ABT-263 displays modest or no single agent activity, it significantly enhances the efficacy of clinically relevant therapeutic regimens.

ABT-239 is a novel, highly efficacious, non-imidazole class of H3R antagonist. Its a transient receptor potential vanilloid type 1 (TRPV1) antagonist.

98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

H2O:insoluble,DMSO:90.0 mg/mL (272.4 mM)

TMN perfusion with ABT-239 activates c-Fos selectively in the NBM and cortex[4]. Perfusion of the TMN with ABT-239 (10 μM) increases histamine release from the TMN, NBM, and cortex, but not from the striatum or NAcc.

ABT-239 (3 mg/kg, i.p.) significantly delays onset of seizure, reduces behavioral seizures elicited by KA, and reduces in the incidence of head bobbing and forelimb clonus in mice. ABT-239 (3 mg/kg, i.p.) administration transforms a short-term learning event into a long-term remembered experience in WT but not in histamine-depleted mice[2]. ABT-239 (3 mg/kg, i.p.) causes enhanced reduction in all the stages. ABT-239 (3 mg/kg, i.p.) and TDZD-8 (10 mg/kg, i.p.) have more powerful reduction in the number of pyknotic neurons in mice hippocampi. ABT-239 (1 mg/kg, i.p.) in conbination with sub-therapeutic dose of SVP (150 mg/kg, i.p.), significantly decreases the number of immobility, head bobbing and forelimb clonus, where as a higher dose combination of The high dose combination of ABT-239 and TDZD-8 produces the most pronounced increase in Bcl-2 expression as well as decrease in the level of Bax[1]. Concomitant administration of either ABT-239 (1 and 3 mg/kg, i.p.) and nicotine (0.035 mg/kg, i.p.), or ABT-239 (0.1 mg/kg, i.p.) and nicotine (0.0175 mg/kg, i.p.) further increases nicotine-induced improvement in both memory acquisition and consolidation[3].

ABT-199 is a Bcl-2-selective inhibitor with Ki of <0.01 nM in cell-free assays, >4800-fold more selective versus Bcl-xL and Bcl-w, and no activity to Mcl-1. Phase 3.

>98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

维奈妥拉;Venetoclax；GDC-0199

Yellow solid

DMSO : 77.5 mg/mL (89.24 mM; Need ultrasonic)

Bcl-2 Family

ABT-199 shows less sensitivity to Bcl-xL, Mcl-1 and Bcl-w with Ki of 48 nM, > 444 nM and 245 nM, respectively. ABT-199 potently inhibits FL5.12-Bcl-2 cells, RS4;11 cells with EC50 of 4 nM and 8 nM, while shows low activity against FL5.12-Bcl-xL cells with EC50 of 261 nM. ABT-199 induces a rapid apoptosis in RS4;11 cells with cytochrome c release, caspase activation, the externalization of phosphatidylserine and the accumulation of sub-G0/G1 DNA. Quantitative immunoblotting reveals that sensitivity to ABT-199 correlated strongly with the expression of Bcl-2, including NHL, DLBCL, MCL, AML and ALL cell lines. ABT-199 also induces apoptosis in CLL with an average EC50 of 3.0 nM.

ABT-199 (100 mg/kg) causes a maximal tumor growth inhibition of 95% and tumor growth delay of 152% in RS4;11 xenografts. ABT-199 also inhibits xenograft growth (DoHH2, Granta-519) as a single agent or in combination with SDX-105 and other agents.