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Signaling Pathway



(ABT-263; ABT 263; ABT263)


Navitoclax Chemical Structure

ABT-263 (Navitoclax) is a potent inhibitor of Bcl-xL, Bcl-2 and Bcl-w with Ki of ≤ 0.5 nM, ≤1 nM and ≤1 nM.

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Free sample   Apply now  
10 mM * 1 mL in DMSO €84 In-stock
5 mg €49 In-stock
10 mg €78 In-stock
25 mg €137 In-stock
50 mg €196 In-stock
100 mg €343 In-stock
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Product name: Navitoclax
Cat. No.: HY-10087

Navitoclax Data Sheet

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    Purity: 98.00%

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Biological Activity of Navitoclax

ABT-263 (Navitoclax) is a potent inhibitor of Bcl-xL, Bcl-2 and Bcl-w with Ki of ≤ 0.5 nM, ≤1 nM and ≤1 nM.
IC50 Value:  ≤ 0.5 nM(Ki for Bcl-xL); ≤1 nM(Ki for Bcl-2); ≤1 nM(Ki for Bcl-w)
Target: Bcl-2 Family
in vitro: 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 <400 nM (H146, H889, H1963, and H1417) are also highly sensitive to ABT-737, and the two most resistant lines (H1048 and H82) are similarly resistant to ABT-263.
in vivo: 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.

Chemical Information

M.Wt 974.61 Storage Please store the product under the recommended conditions in the Certificate of Analysis.
Formula C47H55ClF3N5O6S3
CAS No 923564-51-6
Solvent & Solubility

DMSO ≥190mg/mL Water <1.2mg/mL Ethanol <1.2mg/mL

Preparing Stock Solutions

1 mg 5 mg 10 mg
1 mM 1.0261 mL 5.1303 mL 10.2605 mL
5 mM 0.2052 mL 1.0261 mL 2.0521 mL
10 mM 0.1026 mL 0.5130 mL 1.0261 mL

References on Navitoclax

[1]. Initial testing (stage 1) of the BH3 mimetic ABT-263 by the pediatric preclinical testing program Pediatric Blood & Cancer 50, Pages 1181 – 1189
Background ABT-263 is a potent (Ki?

[2]. Wong M, Tan N, Zha J, Peale FV, Yue P, Fairbrother WJ, Belmont LD.Navitoclax (ABT-263) reduces Bcl-x(L)-mediated chemoresistance in ovarian cancer models.Mol Cancer Ther. 2012 Apr;11(4):1026-35. Epub 2012 Feb 1.
To examine the potential of combining Bcl-2 family inhibitors with chemotherapy in ovarian cancer, we evaluated a panel of 27 ovarian cancer cell lines for response to the combination of navitoclax (formerly ABT-263) and paclitaxel or gemcitabine. The majority of cell lines exhibited a greater than additive response to either combination, as determined by the Bliss independence model, and more than 50% of the ovarian cell lines exhibited strong synergy for the navitoclax/paclitaxel combination. To identify biomarkers for tumors likely to respond to this combination, we evaluated the protein levels of intrinsic apoptosis pathway components. Bcl-x(L) seems necessary, but not sufficient, for navitoclax/paclitaxel synergy in vitro, suggesting that exclusion of patients whose tumors have low or undetectable Bcl-x(L) would enrich for patients responsive to the combination. We evaluated Bcl-x(L) levels in ovarian cancer tumor tissue from 40 patients (20 taxane responsive and 20 with poor response to taxane) and found that patients with high Bcl-x(L) were less sensitive to taxane treatment (10 of 12) Bcl-x(L) positive patients, P = 0.014). These data support the use of navitoclax in combination with taxane-based therapy in ovarian cancer patients with high levels of Bcl-x(L).

[3]. Rudin CM, Hann CL, Garon EB, Ribeiro de Oliveira M, Bonomi PD, Camidge DR, Chu Q, Giaccone G, Khaira D, Ramalingam SS, Ranson MR, Dive C, McKeegan EM, Chyla BJ, Dowell BL, Chakravartty A, Nolan CE, Rudersdorf N, Busman TA, Mabry MH, Krivoshik AP, Humerickhouse RA, Shapiro GI, Gandhi L.Phase II study of single-agent navitoclax (ABT-263) and biomarker correlates in patients with relapsed small cell lung cancer.Clin Cancer Res. 2012 Jun 1;18(11):3163-9. Epub 2012 Apr 11.
PURPOSE: Bcl-2 is a critical regulator of apoptosis that is overexpressed in the majority of small cell lung cancers (SCLC). Nativoclax (ABT-263) is a potent and selective inhibitor of Bcl-2 and Bcl-x(L). The primary objectives of this phase IIa study included safety at the recommended phase II dose and preliminary, exploratory efficacy assessment in patients with recurrent and progressive SCLC after at least one prior therapy. EXPERIMENTAL DESIGN: Thirty-nine patients received navitoclax 325 mg daily, following an initial lead-in of 150 mg daily for 7 days. Study endpoints included safety and toxicity assessment, response rate, progression-free and overall survival (PFS and OS), as well as exploratory pharmacodynamic correlates...

[4]. Ackler S, Mitten MJ, Chen J, Clarin J, Foster K, Jin S, Phillips DC, Schlessinger S, Wang B, Leverson JD, Boghaert ER.Navitoclax (ABT 263) and Bendamustine ± Rituximab Induce Enhanced Killing of Non-Hodgkin's Lymphoma Tumors in Vivo.Br J Pharmacol. 2012 May 24.
Background and Purpose:? Bendamustine with or without rituximab provides an effective and more tolerable alternative to the polytherapy CHOP in the treatment of hematologic tumors, and is currently approved for the treatment of many hematologic malignancies. Navitoclax (ABT 263) is a potent inhibitor of Bcl 2, Bcl x(L) and Bcl w, which has demonstrated efficacy in hematologic tumors alone and in combination with other agents. This paper describes the in vivo efficacy of combining either bendamustine, or bendamustine plus rituximab (BR), with navitoclax in xenograft models of non-Hodgkin's lymphoma Experimental approach:? Activity was tested in xenograft models of diffuse large B-cell lymphoma (DoHH-2, SuDHL-4), mantle cell lymphoma (Granta 519) and Burkitt's lymphoma (RAMOS). Activity was also monitored in a systemic model of Granta 519. Key Results:? Navitoclax potentiates bendamustine activity in all cell lines tested. Bendamustine activated p53 in Granta 519 tumors, concurrent with activation of caspase 3. Navitoclax also improved responses to BR in a subset of tumors. Conclusions and implications:? Navitoclax in combination with bendamustine and BR is a viable combination strategy for use in the clinic, and demonstrated superior efficacy compared to previously reported data for navitoclax plus CHOP and R-CHOP. ? 2012 Abbott Labs. British Journal of Pharmacology ? 2012 The British Pharmacological Society.

[5]. Mérino D, Khaw SL, Glaser SP, Anderson DJ, Belmont LD, Wong C, Yue P, Robati M, Phipson B, Fairlie WD, Lee EF, Campbell KJ, Vandenberg CJ, Cory S, Roberts AW, Ludlam MJ, Huang DC, Bouillet P.Bcl-2, Bcl-x(L), and Bcl-w are not equivalent targets of ABT-737 and navitoclax (ABT-263) in lymphoid and leukemic cells.Blood. 2012 Jun 14;119(24):5807-16. Epub 2012 Apr 26.
The BH3-mimetic ABT-737 and an orally bioavailable compound of the same class, navitoclax (ABT-263), have shown promising antitumor efficacy in preclinical and early clinical studies. Although both drugs avidly bind Bcl-2, Bcl-x(L), and Bcl-w in vitro, we find that Bcl-2 is the critical target in vivo, suggesting that patients with tumors overexpressing Bcl-2 will probably benefit. In human non-Hodgkin lymphomas, high expression of Bcl-2 but not Bcl-x(L) predicted sensitivity to ABT-263. Moreover, we show that increasing Bcl-2 sensitized normal and transformed lymphoid cells to ABT-737 by elevating proapoptotic Bim. In striking contrast, increasing Bcl-x(L) or Bcl-w conferred robust resistance to ABT-737, despite also increasing Bim. Cell-based protein redistribution assays unexpectedly revealed that ABT-737 disrupts Bcl-2/Bim complexes more readily than Bcl-x(L)/Bim or Bcl-w/Bim complexes. These results have profound implications for how BH3-mimetics induce apoptosis and how the use of these compounds can be optimized for treating lymphoid malignancies.

Inhibitor Kit

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