Cat. No.: HY-10087

Navitoclax

Name: Navitoclax
Brand: MedChemExpress
SKU: HY-10087
Price: 50.00 USD
Availability: InStock
Rating: 5 (166 reviews)

(Synonyms: ABT-263)

166 Cited Publications

Customer Review

Based on 166 publication(s) in Google Scholar

Navitoclax (ABT-263 ) is an orally active BH3 mimetic and an inhibitor of Bcl-2, Bcl-xL, and Bcl-w, with a K_i value of <1 nM for each target. Navitoclax triggers endogenous Apoptosis and downregulates the expression of Survivin and TGFβ2. Navitoclax alleviates fibrosis and induces thrombocytopenia. Navitoclax exhibits anticancer activity against a variety of tumors and enhances the efficacy of chemotherapy and radiotherapy. Navitoclax can be used in the research of acute lymphoblastic leukemia, ovarian cancer, and fibrotic diseases.

For research use only. We do not sell to patients.

Purity : 99.64%
CAS No.: 923564-51-6
Formula: C₄₇H₅₅ClF₃N₅O₆S₃
Molecular Weight:974.61

Storage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year

Navitoclax Chemical Structure

CAS No.: 923564-51-6

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Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
- Clinical Trial
Chemical Information
Publications (166)
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
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Biological Activity

Description

IC₅₀ & Target

^[1]

Bcl-2

<1 nM (Ki)

Bcl-xL

<1 nM (Ki)

Bcl-W

<1 nM (Ki)

All Bcl-2 Family Isoforms :

All TGF-β Receptor Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
DMS-79	EC₅₀	0.44 μM Compound: ABT-263	Antiproliferative activity against human DMS 79 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human DMS 79 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
EOL1	EC₅₀	0.011 μM Compound: ABT-263	Antiproliferative activity against human EOL1 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human EOL1 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
FL5.12	EC₅₀	4.2 nM Compound: 2, ABT-263	Cytotoxicity against IL3-dependent mouse FL5.12 cells overexpressing human Bcl-XL assessed as cell viability after 24 hrs by MTS assay in absence of serum Cytotoxicity against IL3-dependent mouse FL5.12 cells overexpressing human Bcl-XL assessed as cell viability after 24 hrs by MTS assay in absence of serum	[PMID: 18841882]
FL5.12	EC₅₀	5.9 nM Compound: 2, ABT-263	Cytotoxicity against IL3-dependent mouse FL5.12 cells overexpressing human Bcl2 assessed as cell viability after 24 hrs by MTS assay in absence of serum Cytotoxicity against IL3-dependent mouse FL5.12 cells overexpressing human Bcl2 assessed as cell viability after 24 hrs by MTS assay in absence of serum	[PMID: 18841882]
GDM-1	EC₅₀	0.011 μM Compound: ABT-263	Antiproliferative activity against human GDM-1 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human GDM-1 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
HEL	EC₅₀	0.07 μM Compound: ABT-263	Antiproliferative activity against human HEL harboring JAK2 V617F mutant assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human HEL harboring JAK2 V617F mutant assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
HL-60	EC₅₀	0.04 μM Compound: ABT-263	Antiproliferative activity against human HL-60 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human HL-60 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
Kasumi 1	EC₅₀	0.03 μM Compound: ABT-263	Antiproliferative activity against human Kasumi 1 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human Kasumi 1 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
KG-1	EC₅₀	0.11 μM Compound: ABT-263	Antiproliferative activity against human KG-1 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human KG-1 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
ML-2	EC₅₀	0.05 μM Compound: ABT-263	Antiproliferative activity against human ML-2 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human ML-2 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
MOLM-13	EC₅₀	0.03 μM Compound: ABT-263	Antiproliferative activity against human MOLM-13 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human MOLM-13 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
MOLM-16	EC₅₀	0.12 μM Compound: ABT-263	Antiproliferative activity against human MOLM16 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human MOLM16 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
MOLT-4	EC₅₀	0.3 μM Compound: 1; ABT-263	Cytotoxicity against human MOLT-4 cells assessed as reduction in cell viability measured after 48 hrs by celltiter-glo assay Cytotoxicity against human MOLT-4 cells assessed as reduction in cell viability measured after 48 hrs by celltiter-glo assay	[PMID: 34141086]
MOLT-4	EC₅₀	112 nM Compound: ABT-263	Antiproliferative activity against Bcl-2 dependent human MOLT-4 cells assessed as reduction in cell viability by measuring effect concentration by CellTiter-Glo reagent based assay Antiproliferative activity against Bcl-2 dependent human MOLT-4 cells assessed as reduction in cell viability by measuring effect concentration by CellTiter-Glo reagent based assay	[PMID: 25787766]
MOLT-4	EC₅₀	303 nM Compound: 21	Antiproliferative activity against human MOLT4 cells in presence of 10% human serum Antiproliferative activity against human MOLT4 cells in presence of 10% human serum	[PMID: 28926247]
MOLT-4	EC₅₀	303 nM Compound: ABT-263	Antiproliferative activity against Bcl-xl dependent human MOLT-4 cells assessed as reduction in cell viability by measuring effect concentration by CellTiter-Glo reagent based assay Antiproliferative activity against Bcl-xl dependent human MOLT-4 cells assessed as reduction in cell viability by measuring effect concentration by CellTiter-Glo reagent based assay	[PMID: 25787766]
MOLT-4	IC₅₀	212.3 nM Compound: ABT-263	Cytotoxicity against human MOLT-4 cells assessed as reduction in cell viability measured after 48 hrs by MTS assay Cytotoxicity against human MOLT-4 cells assessed as reduction in cell viability measured after 48 hrs by MTS assay	[PMID: 34533954]
MV4-11	EC₅₀	0.04 μM Compound: ABT-263	Antiproliferative activity against human MV4-11 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human MV4-11 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
NCI-H1048	EC₅₀	0.9 μM Compound: ABT-263	Antiproliferative activity against human NCI-H1048 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human NCI-H1048 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
NCI-H1417	EC₅₀	0.1 μM Compound: ABT-263	Antiproliferative activity against human NCI-H1417 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human NCI-H1417 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
NCI-H1417	IC₅₀	54.2 nM Compound: 2, ABT-263	Cytotoxicity against human NCI-H1417 cells assessed as growth inhibition after 4 days by WST assay Cytotoxicity against human NCI-H1417 cells assessed as growth inhibition after 4 days by WST assay	[PMID: 23448298]
NCI-H146	EC₅₀	0.08 μM Compound: 2, ABT-263	Cytotoxicity against human NCI-H146 after 48 hrs by MTS assay in presence of 10% human serum Cytotoxicity against human NCI-H146 after 48 hrs by MTS assay in presence of 10% human serum	[PMID: 21366295]
NCI-H146	EC₅₀	86.7 nM Compound: 2, ABT-263	Cytotoxicity against human NCI-H146 cells assessed as cell viability after 48 hrs in presence of 10% human serum Cytotoxicity against human NCI-H146 cells assessed as cell viability after 48 hrs in presence of 10% human serum	[PMID: 18841882]
NCI-H1836	EC₅₀	0.26 μM Compound: ABT-263	Antiproliferative activity against human NCI-H1836 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human NCI-H1836 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
NCI-H187	EC₅₀	0.037 μM Compound: ABT-263	Antiproliferative activity against human NCI-H187 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human NCI-H187 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
NCI-H187	IC₅₀	38.4 nM Compound: 2, ABT-263	Cytotoxicity against human NCI-H187 cells assessed as growth inhibition after 4 days by WST assay Cytotoxicity against human NCI-H187 cells assessed as growth inhibition after 4 days by WST assay	[PMID: 23448298]
NCI-H1963	EC₅₀	0.051 μM Compound: 2, ABT-263	Cytotoxicity against human NCI-H1963 after 48 hrs by MTS assay in presence of 10% human serum Cytotoxicity against human NCI-H1963 after 48 hrs by MTS assay in presence of 10% human serum	[PMID: 21366295]
NCI-H1963	IC₅₀	26.6 nM Compound: 2, ABT-263	Cytotoxicity against human NCI-H1963 cells assessed as growth inhibition after 4 days by WST assay Cytotoxicity against human NCI-H1963 cells assessed as growth inhibition after 4 days by WST assay	[PMID: 23448298]
NCI-H211	EC₅₀	0.1 μM Compound: ABT-263	Antiproliferative activity against human NCI-H211 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human NCI-H211 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
NCI-H345	EC₅₀	0.3 μM Compound: ABT-263	Antiproliferative activity against human NCI-H345 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human NCI-H345 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
NCI-H446	EC₅₀	0.85 μM Compound: ABT-263	Antiproliferative activity against human NCI-H446 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human NCI-H446 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
NCI-H69	EC₅₀	0.18 μM Compound: ABT-263	Antiproliferative activity against human NCI-H69 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human NCI-H69 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
NCI-H889	EC₅₀	0.053 μM Compound: ABT-263	Antiproliferative activity against human NCI-H889 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human NCI-H889 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
NCI-H889	EC₅₀	0.12 μM Compound: 2, ABT-263	Cytotoxicity against human NCI-H889 after 48 hrs by MTS assay in presence of 10% human serum Cytotoxicity against human NCI-H889 after 48 hrs by MTS assay in presence of 10% human serum	[PMID: 21366295]
NOMO-1	EC₅₀	>5 μM Compound: ABT-263	Antiproliferative activity against human NOMO-1 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human NOMO-1 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
OCI-AML2	EC₅₀	0.011 μM Compound: ABT-263	Antiproliferative activity against human OCI-AML2 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human OCI-AML2 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
OCI-AML-3	EC₅₀	>5 μM Compound: ABT-263	Antiproliferative activity against human OCI-AML-3 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human OCI-AML-3 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
OCI-AML-5	EC₅₀	0.18 μM Compound: ABT-263	Antiproliferative activity against human OCI-AML5 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human OCI-AML5 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
Platelet	IC₅₀	0.189 μM Compound: ABT-263	Cytotoxicity against human platelet assessed as cell viability measured after 72 hrs by MTS assay Cytotoxicity against human platelet assessed as cell viability measured after 72 hrs by MTS assay	[PMID: 32388279]
Platelet	IC₅₀	0.325 μM Compound: ABT-263	Cytotoxicity against platelets in human PRP assessed as reduction in cell viability measured after 48 hrs by MTS assay Cytotoxicity against platelets in human PRP assessed as reduction in cell viability measured after 48 hrs by MTS assay	[PMID: 34533954]
RS4-11	EC₅₀	0.014 μM Compound: Navitoclax, ABT-263	Induction of apoptosis in human RS4:11 cells overexpressing BCL-2 assessed as caspase 3/7 activation after 6 hrs by quantitative luminescence assay Induction of apoptosis in human RS4:11 cells overexpressing BCL-2 assessed as caspase 3/7 activation after 6 hrs by quantitative luminescence assay	[PMID: 24881567]
RS4-11	EC₅₀	0.11 μM Compound: 1; ABT-263	Cytotoxicity against human RS4-11 cells assessed as reduction in cell viability measured after 48 hrs by celltiter-glo assay Cytotoxicity against human RS4-11 cells assessed as reduction in cell viability measured after 48 hrs by celltiter-glo assay	[PMID: 34141086]
RS4-11	EC₅₀	112 nM Compound: 21	Antiproliferative activity against human RS4:11 cells in presence of 10% human serum Antiproliferative activity against human RS4:11 cells in presence of 10% human serum	[PMID: 28926247]
RS4-11	IC₅₀	42.6 nM Compound: ABT-263	Cytotoxicity against human RS4-11 cells assessed as reduction in cell viability measured after 48 hrs by MTS assay Cytotoxicity against human RS4-11 cells assessed as reduction in cell viability measured after 48 hrs by MTS assay	[PMID: 34533954]
SET-2	EC₅₀	0.06 μM Compound: ABT-263	Antiproliferative activity against human SET2 harboring JAK2 V617F mutant assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human SET2 harboring JAK2 V617F mutant assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
SIG-M5	EC₅₀	0.011 μM Compound: ABT-263	Antiproliferative activity against human SIG-M5 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human SIG-M5 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
SKM-1	EC₅₀	0.24 μM Compound: ABT-263	Antiproliferative activity against human SKM-1 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human SKM-1 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
THP-1	EC₅₀	0.45 μM Compound: ABT-263	Antiproliferative activity against human THP-1 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay Antiproliferative activity against human THP-1 assessed as reduction in cell viability incubated for 48 hrs by CellTiter-Glo cell vaibility assay	[PMID: 25787766]
WI-38	IC₅₀	8.06 μM Compound: ABT-263	Cytotoxicity against human WI-38 cells assessed as cell viability measured after 72 hrs by MTS assay Cytotoxicity against human WI-38 cells assessed as cell viability measured after 72 hrs by MTS assay	[PMID: 32388279]

In Vitro

Anti-cancerApoptosis

Anti-cancer

Navitoclax (1 nM-10 μM; 96 h) dihydrochloride exhibits cytotoxic activity against a variety of cancer cell lines in vitro, with acute lymphoblastic leukemia (ALL) and Kasumi-1 acute myeloid leukemia (AML) cell lines showing the highest sensitivity (median IC₅₀ for ALL = 0.45 μM, IC₅₀ for RS4;11 cell line = 0.05 μM, IC₅₀ for Kasumi-1 cell line = 0.09 μM). The median IC₅₀ across all tested cell lines is 1.91 μM^[1].
Navitoclax (72 h) dihydrochloride exerts synergistic effects with various chemotherapeutic agents across 46 solid tumor cell lines, with a mean combination index value ranging from 0.05 to 0.75^[2].
When combined with Paclitaxel (HY-B0015), Navitoclax dihydrochloride (14 nM-3 μM; 72 h) exhibits superadditive growth inhibitory effects on 26 out of 27 ovarian cancer cell lines, with strong synergistic effects (Bliss sum >250) observed in 14 cell lines; its single-agent IC₅₀ values range from 0.04 μM in OAW28 cells to 1.3 μM in TOV112D cells^[6].

Anti-cancer

Apoptosis

Navitoclax (1.0 nM-10.0 μM) dihydrochloride exhibits the highest sensitivity toward acute lymphoblastic leukemia (ALL) cell lines among the tested cancer cell lines, and this sensitivity correlates with high expression of BCL-2, BCL-W, BCL-XL and BIM as well as low expression of MCL-1^[4].
Navitoclax dihydrochloride (0.1-25.0 μM; 2 h) induces concentration-dependent Caspase-3 activation in docetaxel (HY-B0011)-pretreated ovarian cancer cells SKOV3^[3].
Navitoclax dihydrochloride binds to purified anti-apoptotic BCL-2 and BCL-XL proteins with high affinity, but does not bind to MCL-1 protein^[4].
Navitoclax dihydrochloride weakly induces apoptosis in BCL-2-deficient cells, indicating that it possesses BCL-2-dependent apoptotic activity^[4].

Apoptosis

Anti-cancer

Navitoclax dihydrochloride potently binds to the anti-apoptotic Bcl-2, Bcl-xL and Bcl-w proteins, with a K_i of <1 nM for each protein^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cytotoxicity Assay^[1]

Cell Line:

23 pediatric cancer cell lines from the Pediatric Preclinical Testing Program (PPTP) in vitro panel, including rhabdomyosarcoma, rhabdoid, Ewing sarcoma, glioblastoma, neuroblastoma, acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), anaplastic large cell lymphoma (ALCL), and non-Hodgkin lymphoma (NHL) lines
Concentration:

1 nM, 10 μM
Incubation Time:

96 h
Result:

Induced cytotoxicity against approximately half of the tested cell lines.
Exhibited a median IC₅₀ of 1.91 μM across all 23 cell lines, with IC₅₀ values ranging from 0.05 μM to >10 μM.
Showed the greatest sensitivity in ALL cell lines, with a median IC₅₀ of 0.45 μM, significantly lower than the median IC₅₀ of >10 μM for non-ALL lines (P=0.02).
Demonstrated high sensitivity in the AML line Kasumi-1, with an IC₅₀ of 0.09 μM.
Had a higher median IC₅₀ of >10 μM in Ewing sarcoma lines compared to non-Ewing lines (median IC₅₀ 1.14 μM, P=0.19).
Achieved IC₅₀ values <1 μM for 9 of the 23 cell lines, a concentration defined as indicative of sensitivity.

Immunofluorescence^[3]

Cell Line:

SKOV3 human ovarian cancer cells
Concentration:

0.1-25.0 μM
Incubation Time:

2 h (following 48 h docetaxel pretreatment)
Result:

Did not increase activated caspase-3 levels alone.
Induced a concentration-dependent increase in the percentage of cells with activated caspase-3 when preceded by docetaxel pretreatment, reaching up to ≈25% at 25.0 μM.

In Vivo

Anti-cancerOthers

Anti-cancer

Navitoclax (100 mg/kg; p.o.; once daily; days 2-21, days 2-3, days 2-15) dihydrochloride shows no efficacy in the SKOV3 ovarian cancer xenograft model, but it significantly enhances the antitumor activity of Docetaxel under various combination and sequential treatment regimens, and improves ORR, TGI and TGD^[2].
Navitoclax (100 mg/kg; p.o.; once daily; for 21 consecutive days) dihydrochloride shows no efficacy in the NCI-H1650 NSCLC xenograft model, but when combined with Erlotinib (HY-50896), it achieves a TGI of 98%, with 100% of the treated mice exhibiting sustained complete remission^[2].

Others

Navitoclax (2-6 mg/kg; p.o.; daily; 2 mg/kg on days 1-6, 6 mg/kg on days 7-12) dihydrochloride induces reversible thrombocytopenia in Beagle dogs, characterized by an initial decrease in platelet count that stabilizes following continuous high-dose treatment, with no bone marrow toxicity^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

Immunocompromised mice (8-10 mice per group; SKOV3 human ovarian cancer cells flank xenograft model)^[2]
Dosage:

100 mg/kg (monotherapy; combination with docetaxel 10 mg/kg; combination with docetaxel 30 mg/kg)
Administration:

p.o.; once daily; 2 days, 14 days, 21 days, days 2-3, days 2-15
Result:

Showed no antitumor efficacy as monotherapy, with negative or minimal TGI values (-44%, -5%, -4% for 21-day, 14-day, and 2-day daily dosing, respectively) and no ORR.
Increased ORR from 30% to 100%, increased TGI from 82% to 92%, and increased TGD from 114% to >175%, with 33% complete regression when combined with docetaxel (10 mg/kg i.v. once every 7 days for 3 cycles) via concurrent 21-day daily dosing.
Increased ORR from 0% to 89%, increased TGI from 48% to 95%, and increased TGD from 12% to 135%, with 56% complete regression when combined with docetaxel (30 mg/kg i.v. once on day 1) via concurrent 14-day daily dosing.
Increased TGI from 48% to 86% and increased TGD from 12% to 54%, with 11% complete regression and 22% ORR when combined with docetaxel (30 mg/kg i.v. once on day 1) via concurrent 2-day daily dosing.
Increased TGI from 48% to 85% and increased TGD from 12% to 38%, with 11% complete regression and 22% ORR when combined with docetaxel (30 mg/kg i.v. once on day 1) via sequential 14-day daily dosing starting on day 2.
Increased TGI from 48% to 63% and increased TGD from 12% to 38%, with no complete regression or ORR when combined with docetaxel (30 mg/kg i.v. once on day 1) via sequential 2-day daily dosing starting on day 2.

Animal Model:

Immunocompromised mice (6 mice per group; NCI-H1650 human NSCLC cells flank xenograft model)^[2]
Dosage:

100 mg/kg (monotherapy; combination with erlotinib 50 mg/kg)
Administration:

p.o.; once daily; 21 days
Result:

Showed no significant antitumor activity as monotherapy.
Increased TGI from 52% to 98%, induced durable complete tumor regressions in 100% of treated mice, and sustained regressions for 25 days after treatment cessation when combined with erlotinib; the combination was well tolerated, with less than 5% body weight loss.

Related Protocols :

Clinical Trial

NCT Number	Sponsor	Condition	Start Date	Phase A549
NCT01329991			2011-05	PHASE1

Chemical Information

CAS No. 923564-51-6
Appearance Solid
Molecular Weight 974.61
Formula C₄₇H₅₅ClF₃N₅O₆S₃
Color White to light yellow
SMILES

O=S(C1=CC(S(NC(C2=CC=C(N3CCN(CC4=C(CCC(C)(C4)C)C5=CC=C(Cl)C=C5)CC3)C=C2)=O)(=O)=O)=CC=C1N[C@H](CCN6CCOCC6)CSC7=CC=CC=C7)(C(F)(F)F)=O
Synonyms

ABT-263
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	2 years
	-20°C	1 year

Publications (166)

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Signal Transduct Target Ther

Selective depletion of tumor-associated SAMHD1 enhances chemotherapeutic efficacy and antitumor immune responses. [Abstract]

2025 Dec 15;10(1):406. PMID: 41392286
Cancer Cell

CCL3 is produced by aged neutrophils across cancers and promotes tumor growth. [Abstract]

2026 Feb 5:S1535-6108(26)00045-0. PMID: 41650972
Cancer Cell

Senescence Reprogramming by TIMP1 Deficiency Promotes Prostate Cancer Metastasis. [Abstract]

2021 Jan 11;39(1):68-82.e9. PMID: 33186519
Cell

Inhibition of oligomeric BAX by an anti-apoptotic dimer. [Abstract]

2025 Dec 24;188(26):7397-7412.e21. PMID: 41274283
Cell Res

Antagonizing the irreversible thrombomodulin-initiated proteolytic signaling alleviates age-related liver fibrosis via senescent cell killing. [Abstract]

2023 Jul;33(7):516-532. PMID: 37169907
Cancer Discov

Targeting KRAS codon 13 mutations using direct combination approaches in non-small cell lung cancer. [Abstract]

2026 Jun 22. PMID: 42329102
Cancer Discov

P21-positive senescent stromal cells promote prostate cancer immune suppression and progression that can be reversed by senolytic therapy. [Abstract]

2025 Oct 27. PMID: 41135083
Nat Genet

Chromothripsis-associated chromosome 21 amplification orchestrates transformation to blast-phase MPN through targetable overexpression of DYRK1A. [Abstract]

2025 Jun;57(6):1478-1492. PMID: 40490510
Cell Stem Cell

Senolytic-sensitive p16Ink4a+ fibroblasts in the tumor stroma rewire lung cancer metabolism and plasticity. [Abstract]

2025 Dec 4;32(12):1869-1885.e8. PMID: 41187746
Nat Cell Biol

p53 increases phospholipid headgroup scavenging in senescence. [Abstract]

2026 Feb;28(2):296-306. PMID: 41501178
Cancer Res

ETC-501 is a Brain Penetrant MNK Kinase Inhibitor that Potentiates TMZ-Induced Senescence and Sensitizes Glioblastoma Cells to Senolytic Therapy. [Abstract]

2026 Jan 22. PMID: 41570320
Cancer Res

H4K20me3-Mediated Repression of Inflammatory Genes Is a Characteristic and Targetable Vulnerability of Persister Cancer Cells. [Abstract]

2025 Jan 2;85(1):32-51. PMID: 39476057
Nat Commun

Systematic profiling reveals distinct senescence signatures and regulators across human brain cell types. [Abstract]

2025 Dec 11;16(1):11059. PMID: 41381419
Nat Commun

Remodeling of the immune microenvironment is linked to adverse outcome in pediatric T cell acute lymphoblastic leukemia. [Abstract]

2025 Nov 21;16(1):10263. PMID: 41271691
Nat Commun

Diabetes reshapes pancreatic cancer-associated endothelial niche by accelerating senescence. [Abstract]

2025 Sep 30;16(1):8654. PMID: 41027967
Nat Commun

Proapoptotic Bcl-2 inhibitor as potential host directed therapy for pulmonary tuberculosis. [Abstract]

2025 Mar 27;16(1):3003. PMID: 40148277
Nat Commun

Integrated molecular and functional characterization of the intrinsic apoptotic machinery identifies therapeutic vulnerabilities in glioma. [Abstract]

2024 Nov 21;15(1):10089. PMID: 39572533
Nat Commun

Senescence drives immunotherapy resistance by inducing an immunosuppressive tumor microenvironment. [Abstract]

2024 Mar 18;15(1):2435. PMID: 38499573
Nat Commun

ABCC1 and glutathione metabolism limit the efficacy of BCL-2 inhibitors in acute myeloid leukemia. [Abstract]

2023 Sep 19;14(1):5709. PMID: 37726279
Nat Commun

Systematic characterization of cancer transcriptome at transcript resolution. [Abstract]

2022 Nov 10;13(1):6803. PMID: 36357395

Navitoclax purchased from MedChemExpress. Usage Cited in: Nat Commun. 2022 Nov 10;13(1):6803. [Abstract]

Navitoclax (0.5-1.5 μM;10 d) combined with decitabine significantly reduces the transcriptional activity of KIAA1522-a6 in siPTBP1-transfected A2780 cells.
Nat Commun

Single-cell transcriptomics identifies Mcl-1 as a target for senolytic therapy in cancer. [Abstract]

2022 Apr 21;13(1):2177. PMID: 35449130
Nat Commun

Co-targeting of BAX and BCL-XL proteins broadly overcomes resistance to apoptosis in cancer. [Abstract]

2022 Mar 7;13(1):1199. PMID: 35256598
Nat Commun

Oncogenic enhancers drive esophageal squamous cell carcinogenesis and metastasis. [Abstract]

2021 Jul 22;12(1):4457. PMID: 34294701
Nat Commun

A BET family protein degrader provokes senolysis by targeting NHEJ and autophagy in senescent cells. [Abstract]

2020 Apr 22;11(1):1935. PMID: 32321921
Nat Commun

Pharmacological reactivation of MYC-dependent apoptosis induces susceptibility to anti-PD-1 immunotherapy. [Abstract]

2019 Feb 6;10(1):620. PMID: 30728358
Circ Res

Endothelial FUNDC1 Deficiency Drives Pulmonary Hypertension. [Abstract]

2025 Jan 17;136(2):e1-e19. PMID: 39655444
Cell Discov

Lineage-coupled clonal capture identifies clonal evolution mechanisms and vulnerabilities of BRAFV600E inhibition resistance in melanoma. [Abstract]

2022 Oct 6;8(1):102. PMID: 36202798

Navitoclax purchased from MedChemExpress. Usage Cited in: Cell Discov. 2022 Oct 6;8(1):102. [Abstract]

Cell viability of the captured clones in response to ABT263 (Navitoclax) (2 days). Results are representative of two independent experiments with three technical replicates per experiment, and error bars represent SEM.
Sci Transl Med

Hematopoietic loss of Y chromosome activates immune checkpoints and contributes to impaired senescent cell clearance and renal disease. [Abstract]

2025 Aug 6;17(810):eadv4071. PMID: 40768598
Sci Transl Med

PP2A inhibition is a druggable MEK inhibitor resistance mechanism in KRAS-mutant lung cancer cells. [Abstract]

2018 Jul 18;10(450):eaaq1093. PMID: 30021885
J Exp Clin Cancer Res

HSF1 is a prognostic determinant and therapeutic target in intrahepatic cholangiocarcinoma. [Abstract]

2024 Sep 6;43(1):253. PMID: 39243039

Navitoclax purchased from MedChemExpress. Usage Cited in: J Exp Clin Cancer Res. 2024 Sep 6;43(1):253. [Abstract]

The co-treatment with ABT-263 (Navitoclax) (0.2 μM) and KRIBB-11 inhibits the cell viability in iCCA hCAFs. Effect of ABT-263, KRIBB-11, and their co-administration on the viability of iCCA hCAFs, grown for 72 h in culture medium supplemented with 10% FBS. Note the higher anti-growth effects of the two combined drugs than single treatments.
Adv Sci (Weinh)

Beyond CD30: Dual-Targeting of Malignant and Regulatory T Cells by Brentuximab Vedotin Remodels the Lymphoma Microenvironment and Overcomes Resistance via BCL2 Inhibition in Mycosis Fungoides. [Abstract]

2026 Feb 28:e17353. PMID: 41762706
NPJ Aging

AI-aided identification of dual-purpose therapeutic targets PRPF19 and MAPK9 in hepatocellular carcinoma and cellular senescence. [Abstract]

2025 Dec 17;11(1):101. PMID: 41407697
NPJ Aging

Increased vascular smooth muscle cell senescence in aneurysmal Fibulin-4 mutant mice. [Abstract]

2024 Jun 20;10(1):31. PMID: 38902222
J Control Release

The HSP90-dependent bioorthogonal PROTAC prodrug system enables tumor-selective and enhanced protein degradation. [Abstract]

2026 May 10:393:114828. PMID: 41839264
J Control Release

Fluorinated albumin nanocages dually target CAFs and tumor cells to potentiate bladder cancer chemoimmunotherapy. [Abstract]

2025 Nov 10:387:114246. PMID: 40972824
Cell Death Dis

2026 Apr 10;17(1):388.
Cell Death Dis

Repurposing BCL2 inhibitors: Venetoclax protects against acinar cell necrosis in acute pancreatitis by promoting apoptosis. [Abstract]

2025 Jul 27;16(1):566. PMID: 40715042
Cell Death Dis

Disrupting pro-survival and inflammatory pathways with dimethyl fumarate sensitizes chronic lymphocytic leukemia to cell death. [Abstract]

2024 Mar 18;15(3):224. PMID: 38494482
Pharmacol Res

Combination of palbociclib with navitoclax based-therapies enhances in vivo antitumoral activity in triple-negative breast cancer. [Abstract]

2023 Jan:187:106628. PMID: 36566002
Cell Death Dis

Constitutive BAK/MCL1 complexes predict paclitaxel and S63845 sensitivity of ovarian cancer. [Abstract]

2021 Aug 12;12(8):789. PMID: 34385422
Cell Death Dis

ETV7 regulates breast cancer stem-like cell features by repressing IFN-response genes. [Abstract]

2021 Jul 27;12(8):742. PMID: 34315857
Cell Death Dis

MCL1 inhibitors S63845/MIK665 plus Navitoclax synergistically kill difficult-to-treat melanoma cells. [Abstract]

2020 Jun 8;11(6):443. PMID: 32513939
Cell Death Dis

Chemotherapy-induced pyroptosis is mediated by BAK/BAX-caspase-3-GSDME pathway and inhibited by 2-bromopalmitate. [Abstract]

2020 Apr 24;11(4):281. PMID: 32332857
Cell Death Dis

MCL1 inhibition is effective against a subset of small-cell lung cancer with high MCL1 and low BCL-XL expression. [Abstract]

2020 Mar 9;11(3):177. PMID: 32152266
Cell Death Dis

CDK7 inhibitor THZ1 inhibits MCL1 synthesis and drives cholangiocarcinoma apoptosis in combination with BCL2/BCL-XL inhibitor ABT-263. [Abstract]

2019 Aug 9;10(8):602. PMID: 31399555
Cell Death Dis

Sensitizing non-small cell lung cancer to BCL-xL-targeted apoptosis. [Abstract]

2018 Sep 24;9(10):986. PMID: 30250075

Navitoclax purchased from MedChemExpress. Usage Cited in: Cell Death Dis. 2018 Sep 24;9(10):986. [Abstract]

Cells are treated with 25 nM siRNA for 48 hours followed by 1 μM ABT-263 for 36 hours.
Cell Commun Signal

Chemotherapy-induced senescent nasopharyngeal carcinoma cells suppress NK cell-mediated antitumor immunity by upregulating EBI3 via mtDNA-cGAS-STING pathway. [Abstract]

2026 Mar 28;24(1):279. PMID: 41904509
Cell Commun Signal

ONC212, alone or in synergistic conjunction with Navitoclax (ABT-263), promotes cancer cell apoptosis via unconventional mitochondrial-independent caspase-3 activation. [Abstract]

2024 Sep 13;22(1):441. PMID: 39272099
Adv Healthc Mater

Local Delivery of Senolytic Drug Inhibits Intervertebral Disc Degeneration and Restores Intervertebral Disc Structure. [Abstract]

2022 Jan;11(2):e2101483. PMID: 34699690
Cell Death Discov

Exploiting dysregulated iron homeostasis to eradicate persistent high-grade serous ovarian cancer. [Abstract]

2025 Sep 25;11(1):423. PMID: 40998801
Acta Pharmacol Sin

Chromosome instability functions as a potential therapeutic reference by enhancing chemosensitivity to BCL-XL inhibitors in colorectal carcinoma. [Abstract]

2024 Nov;45(11):2420-2431. PMID: 39187678
Acta Biomater

A navitoclax-loaded nanodevice targeting matrix metalloproteinase-3 for the selective elimination of senescent cells. [Abstract]

2024 Mar 1:176:405-416. PMID: 38185231
Cell Death Discov

A novel BH3 mimetic Bcl-2 inhibitor promotes autophagic cell death and reduces in vivo Glioblastoma tumor growth. [Abstract]

2022 Oct 29;8(1):433. PMID: 36309485
Acta Biomater

Local delivery of a senolytic drug in ischemia and reperfusion-injured heart attenuates cardiac remodeling and restores impaired cardiac function. [Abstract]

2021 Nov:135:520-533. PMID: 34454081
Leukemia

BET inhibitor-based combinations targeting novel dependencies in MECOM-rearranged (r) AML. [Abstract]

2025 Dec 19. PMID: 41419608
Leukemia

Combining MCL-1 inhibition and CD37-directed chimeric antigen receptor T cells as an effective strategy to target T-cell lymphoma. [Abstract]

2025 Jul 30. PMID: 40739330
Leukemia

Altered RNA export by SF3B1 mutants confers sensitivity to nuclear export inhibition. [Abstract]

2024 Sep;38(9):1894-1905. PMID: 38997434
Free Radic Biol Med

FMO1 disrupts mitochondrial functional homeostasis through ROS-mediated mechanisms to drive chondrocyte senescence and hypertrophy. [Abstract]

2026 Aug 16:252:613-624. PMID: 42105790
Stem Cell Res Ther

Senolysis potentiates endothelial progenitor cell adhesion to and integration into the brain vasculature. [Abstract]

2024 Nov 11;15(1):413. PMID: 39529098
Am J Chin Med

Salvianolic Acid Ameliorates Pressure Overload-Induced Cardiac Endothelial Dysfunction via Activating HIF1[Formula: see text]/HSF1/CD31 Pathway. [Abstract]

2022;50(7):1869-1885. PMID: 36121714
Stem Cell Res Ther

Clearance of senescent cells with ABT-263 improves biological functions of synovial mesenchymal stem cells from osteoarthritis patients. [Abstract]

2022 Jun 3;13(1):222. PMID: 35658936
Cell Rep

Dual blockade of PD-1 and NKG2A prevents NK cell senescence and reprograms the immunosuppressive microenvironment in pancreatic cancer. [Abstract]

2026 Jun 20;45(7):117583. PMID: 42322608
Aging Cell

Morphofunctional Heterogeneity and Plasticity of Glioblastoma Cells Induced to Senescence by Temozolomide. [Abstract]

2026 Apr;25(4):e70477. PMID: 41963773
Aging Cell

2026 Jan 20;25(2):e70352.
Blood Adv

Preclinical efficacy of tasquinimod-based combinations in advanced myeloproliferative neoplasms (MPN) in blastic phase. [Abstract]

2025 Aug 19:bloodadvances.2025016898. PMID: 40829105
Blood Adv

BH3 mimetic drugs overcome the microenvironment-induced resistance to crizotinib in ALK+ anaplastic large cell lymphoma. [Abstract]

2025 Jul 2:bloodadvances.2024015322. PMID: 40601898
Cell Rep

Divergent sex-specific effects on a ketogenic diet: Male, but not female, mice exhibit oxidative stress and cellular senescence. [Abstract]

2025 Jul 17;44(8):116026. PMID: 40682777
Aging Cell

Investigating the Role of TRPV4 and GPR35 Interaction in Endothelial Dysfunction in Aging Mice. [Abstract]

2025 May;24(5):e14469. PMID: 39744893
Aging Cell

Cellular senescence contributes to spontaneous repair of the rat meniscus. [Abstract]

2025 Feb;24(2):e14385. PMID: 39439195
Blood Adv

CBFA2T3::GLIS2 Pediatric Acute Megakaryoblastic Leukemia is Sensitive to BCL-XL Inhibition by Navitoclax and DT2216. [Abstract]

2024 Jan 9;8(1):112-129. PMID: 37729615
Cell Rep

BCL-xL inhibition potentiates cancer therapies by redirecting the outcome of p53 activation from senescence to apoptosis. [Abstract]

2022 Dec 20;41(12):111826. PMID: 36543138
Neurotherapeutics

Transcriptionally distinct malignant neuroblastoma populations show selective response to adavosertib treatment. [Abstract]

2025 Apr;22(3):e00575. PMID: 40118716
J Med Chem

Systems Biology-Based Drug Repositioning Identifies Extracellular Matrix Module as a Therapeutic Target in Lung Squamous Cell Carcinoma. [Abstract]

2025 Oct 17. PMID: 41105954
Sci Data

High-throughput drug screening identifies novel therapeutics for Low Grade Serous Ovarian Carcinoma. [Abstract]

2024 Sep 19;11(1):1024. PMID: 39300112
Sci Signal

Metabolic perturbations sensitize triple-negative breast cancers to apoptosis induced by BH3 mimetics. [Abstract]

2021 Jun 8;14(686):eabc7405. PMID: 34103421
Sci Signal

High-throughput dynamic BH3 profiling may quickly and accurately predict effective therapies in solid tumors. [Abstract]

2020 Jun 16;13(636):eaay1451. PMID: 32546544
Mol Cancer Ther

Harnessing senolytics and PARP inhibition to expand the antitumor activity of CDK4/6 inhibitors in prostate cancer. [Abstract]

2025 Jul 2. PMID: 40601842
Pharmaceutics

Targeted Drug Therapy for Senescent Cells Alleviates Unilateral Ureteral Obstruction-Induced Renal Injury in Rats. [Abstract]

2024 May 23;16(6):695. PMID: 38931822
Pharmaceutics

Maximizing Anticancer Response with MPS1 and CENPE Inhibition Alongside Apoptosis Induction. [Abstract]

2023 Dec 29;16(1):56. PMID: 38258067
Mol Cancer Ther

Bepotastine sensitizes ovarian cancer to PARP inhibitors through suppressing NF-κB-triggered SASP in cancer-associated fibroblasts. [Abstract]

2023 Apr 3;22(4):447-458. PMID: 36780236
Pharmaceutics

Navitoclax Enhances the Therapeutic Effects of PLK1 Targeting on Lung Cancer Cells in 2D and 3D Culture Systems. [Abstract]

2022 Jun 6;14(6):1209. PMID: 35745782
JCI Insight

OGDH and Bcl-xL loss causes synthetic lethality in glioblastoma. [Abstract]

2024 Mar 14;9(8):e172565. PMID: 38483541
JCI Insight

Inhibition of antiapoptotic BCL-2 proteins with ABT-263 induces fibroblast apoptosis, reversing persistent pulmonary fibrosis. [Abstract]

2023 Feb 8;8(3):e163762. PMID: 36752201
Biochem Pharmacol

Senolytic elimination of therapy-induced senescent cells by ABT-263 improves chemotherapeutic efficacy in esophageal squamous cell carcinoma. [Abstract]

2026 Mar:245:117659. PMID: 41423036
Cells

2026 Jan 16;15(2):164.
Geroscience

The senolytic ABT-263 improves cognitive functions in middle-aged male, but not female, atherosclerotic LDLr-/-;hApoB100+/+ mice. [Abstract]

2025 Jun;47(3):4577-4600. PMID: 39982668
Int J Pharm

Co-encapsulation of PI3-Kδ/HDAC6 dual inhibitor and Navitoclax in Quatramer™ nanoparticles for synergistic effect in ER+ breast cancer. [Abstract]

2022 Nov 25:628:122343. PMID: 36341921
Cells

EA.hy926 Cells and HUVECs Share Similar Senescence Phenotypes but Respond Differently to the Senolytic Drug ABT-263. [Abstract]

2022 Jun 21;11(13):1992. PMID: 35805077
Acs Biomater Sci Eng

A Senolytic-Eluting Coronary Stent for the Prevention of In-Stent Restenosis. [Abstract]

2022 May 9;8(5):1921-1929. PMID: 35416659
Cells

Selective Targeting of Cancer-Associated Fibroblasts by Engineered H-Ferritin Nanocages Loaded with Navitoclax. [Abstract]

2021 Feb 5;10(2):328. PMID: 33562504
Biomacromolecules

Injectable Senolytic Hydrogel Depot for the Clearance of Senescent Cells. [Abstract]

2025 Feb 10;26(2):814-824. PMID: 39783796
Acta Physiol

Tacrolimus Induced Hypertension and Vascular Remodeling Includes Mechanisms of Cellular Senescence-The Protective Effect of Valsartan. [Abstract]

2026 Apr;242(4):e70189. PMID: 41814130
Reprod Biol Endocrinol

A novel senotherapeutic strategy with azithromycin for preventing endometriosis progression. [Abstract]

2025 Mar 26;23(1):47. PMID: 40140889
Pharmaceuticals (Basel)

A Novel Regimen for Treating Melanoma: MCL1 Inhibitors and Azacitidine. [Abstract]

2021 Jul 30;14(8):749. PMID: 34451846
Int J Mol Sci

2026 Aug 17;27(16):7359. PMID: 42653363
Biomolecules

Targeting Cellular Senescence to Enhance Human Endometrial Stromal Cell Decidualization and Inhibit Their Migration. [Abstract]

2025 Jun 16;15(6):873. PMID: 40563513
Int J Mol Sci

The Differential Effect of Senolytics on SASP Cytokine Secretion and Regulation of EMT by CAFs. [Abstract]

2024 Apr 4;25(7):4031. PMID: 38612842
Int J Mol Sci

Developing 3D Organoid Raft Cultures from Patient-Derived Xenografts as Rapid Models to Screen Efficacy of Experimental Therapeutics. [Abstract]

2022 Nov 19;23(22):14392. PMID: 36430867
J Integr Med

Morin inhibits ubiquitination degradation of BCL-2 associated agonist of cell death and synergizes with BCL-2 inhibitor in gastric cancer cells. [Abstract]

2025 Apr 22:S2095-4964(25)00050-0. PMID: 40319008
Toxicology

Proteasome inhibition induces apoptosis through simultaneous inactivation of MCL-1/BCL-XL by NOXA independent of CHOP and JNK pathways. [Abstract]

2024 Nov:508:153906. PMID: 39117261
Mol Med Rep

Inhibition of Bcl-2 and Bcl-xL overcomes the resistance to the third-generation EGFR tyrosine kinase inhibitor osimertinib in non-small cell lung cancer. [Abstract]

2021 Jan;23(1):48. PMID: 33200796
Cancers (Basel)

Antineoplastic Drug Synergy of Artesunate with Navitoclax in Models of High-Grade Serous Ovarian Cancer. [Abstract]

2024 Mar 28;16(7):1321. PMID: 38610999
Cancers (Basel)

Tumor-Associated Fibroblast-Derived Exosomal circDennd1b Promotes Pituitary Adenoma Progression by Modulating the miR-145-5p/ONECUT2 Axis and Activating the MAPK Pathway. [Abstract]

2023 Jun 27;15(13):3375. PMID: 37444485
Comput Struct Biotechnol J

A deep tabular data learning model predicting cisplatin sensitivity identifies BCL2L1 dependency in cancer. [Abstract]

2023 Jan 16:21:956-964. PMID: 36733702
Neoplasia

Mcl-1 levels critically impact the sensitivities of human colorectal cancer cells to APG-1252-M1, a novel Bcl-2/Bcl-XL dual inhibitor that induces Bax-dependent apoptosis. [Abstract]

2022 Jul;29:100798. PMID: 35462114
Sens Biosensing Res

2026 Aug 14;53:101074.
J Cell Mol Med

Inactivation of CDK12 Enhances Mitochondrial Efficiency to Suppress DNA Damage. [Abstract]

2026 Apr;30(7):e71101. PMID: 41896195
J Cell Mol Med

LAPTM5 Confers the Resistance to Venetoclax via Promoting the Autophagosome-Lysosome Fusion in Multiple Myeloma. [Abstract]

2025 Jan;29(1):e70331. PMID: 39753521
Mol Cell Biochem

Bcl-2/Bcl-xL inhibitor navitoclax increases the antitumor effect of Chk1 inhibitor prexasertib by inducing apoptosis in pancreatic cancer cells via inhibition of Bcl-xL but not Bcl-2. [Abstract]

2020 Sep;472(1-2):187-198. PMID: 32567031
iScience

Developing therapeutic strategies to target MCL1 and BCLXL in lethal prostate cancer. [Abstract]

2025 Nov 10;28(12):113985. PMID: 41438049
Mol Oncol

The CDK12-BRCA1 signaling axis mediates dinaciclib-associated radiosensitivity through p53-mediated cellular senescence. [Abstract]

2025 Apr;19(4):1265-1280. PMID: 39626031
Neurochem Res

Neuroblastoma SH-SY5Y Cell Differentiation to Mature Neuron by AM580 Treatment. [Abstract]

2022 Dec;47(12):3723-3732. PMID: 36066699
iScience

Reciprocal effects of mTOR inhibitors on pro-survival proteins dictate therapeutic responses in tuberous sclerosis complex. [Abstract]

2022 Oct 28;25(11):105458. PMID: 36388985
Nanomedicine

Polylactic acid based polymeric nanoparticle mediated co-delivery of navitoclax and decitabine for cancer therapy. [Abstract]

2023 Jan:47:102627. PMID: 36410699
J Infect Dis

Elimination of HIV Reservoirs Harboring Intact Proviruses. [Abstract]

2025 Jul 16:jiaf373. PMID: 40668935
Ther Adv Med Oncol

Navitoclax combined with Alpelisib effectively inhibits Merkel cell carcinoma cell growth in vitro. [Abstract]

2020 Dec 14:12:1758835920975621. PMID: 33403016
Development

Dysfunction of programmed embryo senescence is linked to genetic developmental defects. [Abstract]

2023 May 1;150(9):dev200903. PMID: 37017267
ACS Med Chem Lett

High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma. [Abstract]

2015 Jun 22;6(8):948-52. PMID: 26288699

Navitoclax purchased from MedChemExpress. Usage Cited in: ACS Med Chem Lett. 2015 Jun 22;6(8):948-52. [Abstract]

Combination treatment. (a) Comparison of AZD-8055 and ABT-263 treatment in all cell lines. Red indicates sensitivity, while blue indicates resistance. (b) Depiction of synergism where the values shown are excess over Bliss Independence, a prediction of inhibition without synergism. Increased synergism is evident by an increased number, shown in red, while negative numbers in blue represent an antagonistic effect.
Biochim Biophys Acta Gene Regul Mech

DNA-PKcs as an upstream mediator of OCT4-induced MYC activation in small cell lung cancer. [Abstract]

2023 Apr 26;1866(2):194939. PMID: 37116859
Toxicol Appl Pharmacol

Gestational arsenite exposure augments hepatic tumors of C3H mice by promoting senescence in F1 and F2 offspring via different pathways. [Abstract]

2020 Dec 1:408:115259. PMID: 33010264
ChemMedChem

Advancing Accurate Quantification of Protein-Ligand Interactions: Differential Scanning Calorimetry as a Precision Screening Tool Using BCL-2 as a Model System. [Abstract]

2026 Mar 13;21(5):e202500744. PMID: 41774457
Cancer Med

Identification and Validation of cGAS-STING Pathway-Associated Predictive and Therapeutic Models for Esophageal Squamous Cell Cancer Patients via Artificial Intelligence and Multi-Omics. [Abstract]

2026 Mar;15(3):e71645. PMID: 41731722
Mol Carcinog

Therapeutic potential of the novel Bcl-2/Bcl-XL dual inhibitor, APG1252, alone or in combination against non-small cell lung cancer. [Abstract]

2022 Nov;61(11):1031-1042. PMID: 36066010
Pigment Cell Melanoma Res

Establishment and characterization of an immortalized human giant congenital melanocytic nevi cell line. [Abstract]

2022 May;35(3):356-368. PMID: 35218152
Breast Cancer Res Treat

Dual targeting of HSP90 and BCL-2 in breast cancer cells using inhibitors BIIB021 and ABT-263. [Abstract]

2025 Apr;210(2):493-506. PMID: 39779635
Breast Cancer Res Treat

Rationally derived drug combinations with the novel Mcl-1 inhibitor EU-5346 in breast cancer. [Abstract]

2019 Feb;173(3):585-596. PMID: 30374681
Am J Cancer Res

Targeting sphingosine kinase 2 suppresses cell growth and synergizes with BCL2/BCL-XL inhibitors through NOXA-mediated MCL1 degradation in cholangiocarcinoma. [Abstract]

2019 Mar 1;9(3):546-561. PMID: 30949409
PLoS One

Synergistic apoptotic effects in cancer cells by the combination of CLK and Bcl-2 family inhibitors. [Abstract]

2020 Oct 16;15(10):e0240718. PMID: 33064779
FEBS Open Bio

PARP inhibitors induce a senescence phenotype in non-small cell lung carcinoma cell lines. [Abstract]

2026 Feb 19. PMID: 41714887
Biochem Biophys Res Commun

The deubiquitinating enzyme USP20 regulates the stability of the MCL1 protein. [Abstract]

2022 Feb 19:593:122-128. PMID: 35063767
J Chromatogr Sci

Simultaneous Bioanalytical Method Development and Validation of Navitoclax and Doxorubicin in Rat Plasma Using UHPLC-HESI-LTQ-MS. [Abstract]

2025 Aug 30;63(8):bmaf046. PMID: 40884358
Melanoma Res

Combined Mcl-1 and YAP1/TAZ inhibition for treatment of metastatic uveal melanoma. [Abstract]

2023 Oct 1;33(5):345-356. PMID: 37467061
Biomed Pharmacother

2026 Sep:202:119803. PMID: 42537395
bioRxiv

2026 Aug 4.
Res Sq

2026 Aug 29.
McGill University

2026.
Masaryk University

2026.
bioRxiv

2026 Jun 26.
bioRxiv

2026 Jun 30.
bioRxiv

Sacituzumab Govitecan as an Effective Strategy for Sensitizing Chemoresistant HNSCC Cells to Senolytic Intervention. [Abstract]

2026 Apr 15:2026.04.13.718209. PMID: 42039381
Res Sq

2026 Jan 15.
SSRN

2025 Oct 15.
bioRxiv

BOGO: A Proteome-Wide Gene Overexpression Platform for Discovering Rational Cancer Combination Therapies. [Abstract]

2025 Sep 7:2025.09.02.673780. PMID: 40950237
University of Szeged

2025.
Seoul National University

2025.
University of Montreal

2025.
Research Square Print

2025 May 28.
University of Washington

2025.
bioRxiv

Regulatory Network Inference of Induced Senescent Midbrain Cell Types Reveals Cell Type-Specific Senescence-Associated Transcriptional Regulators. [Abstract]

2025 Feb 6:2025.02.06.636893. PMID: 39975267
bioRxiv

2024 Jul 25.
Res Sq

BMP receptor 2 inhibition regulates mitochondrial bioenergetics to induce synergistic cell death with BCL-2 inhibitors in leukemia and NSLC cells. [Abstract]

2024 Sep 12:rs.3.rs-5065904. PMID: 39315260
Res Sq

Proapoptotic Bcl-2 inhibitor as host directed therapy for pulmonary tuberculosis. [Abstract]

2024 Sep 2:rs.3.rs-4926508. PMID: 39281866
bioRxiv

Senescent fibroblasts in the tumor stroma rewire lung cancer metabolism and plasticity. [Abstract]

2024 Jul 30:2024.07.29.605645. PMID: 39131266
McGill University

2023 Dec.
bioRxiv

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University of Michigan

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Research Square Preprint

2023 Jul 26.
Patent

US20220062383A1.
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Biomed Pharmacother

Foeniculum vulgare seed extract induces apoptosis in lung cancer cells partly through the down-regulation of Bcl-2. [Abstract]

2021 Mar:135:111213. PMID: 33395604
University of Colorado

2020 Dec.
Biomed Pharmacother

Triptolide impairs genome integrity by directly blocking the enzymatic activity of DNA-PKcs in human cells. [Abstract]

2020 Sep:129:110427. PMID: 32574974
Norwegian University of Science and Technology

2020 Jul.
Aging (Albany NY)

Transient metabolic improvement in obese mice treated with navitoclax or dasatinib/quercetin. [Abstract]

2020 Jun 25;12(12):11337-11348. PMID: 32584785
University of Michigan

2020 May.

Solvent & Solubility

In Vitro:

DMSO : 100 mg/mL (102.61 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

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

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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Dilution Calculator

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.5 mg/mL (2.57 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (299 KB)
SDS (396 KB)
- English - EN (396 KB)
- Français - FR (396 KB)
- Deutsch - DE (396 KB)
- Norwegian - NO (396 KB)
- Español - ES (396 KB)
- Swedish - SV (396 KB)
- Italian - IT (396 KB)
- Korean - KR (396 KB)
- Portuguese - PT (396 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Lock R, et al. Initial testing (stage 1) of the BH3 mimetic ABT-263 by the pediatric preclinical testing program. Pediatric blood & cancer. 2008 Jun;50(6):1181-9. [Content Brief]

[2]. Chen J, et al. The Bcl-2/Bcl-X(L)/Bcl-w inhibitor, navitoclax, enhances the activity of chemotherapeutic agents in vitro and in vivo. Mol Cancer Ther. 2011 Dec;10(12):2340-9. [Content Brief]

[3]. Chen J, et al. The Bcl-2/Bcl-X(L)/Bcl-w inhibitor, navitoclax, enhances the activity of chemotherapeutic agents in vitro and in vivo. Molecular cancer therapeutics. 2011 Dec;10(12):2340-9. [Content Brief]

[4]. Mohamad Anuar NN, et al. Clinical Review: Navitoclax as a Pro-Apoptotic and Anti-Fibrotic Agent. Frontiers in pharmacology. 2020;11:564108. [Content Brief]

[5]. Wilson WH, et al. Navitoclax, a targeted high-affinity inhibitor of BCL-2, in lymphoid malignancies: a phase 1 dose-escalation study of safety, pharmacokinetics, pharmacodynamics, and antitumour activity. The Lancet. Oncology. 2010 Dec;11(12):1149-59. [Content Brief]

[6]. Wong M, et al. Navitoclax (ABT-263) reduces Bcl-x(L)-mediated chemoresistance in ovarian cancer models. Molecular cancer therapeutics. 2012 Apr;11(4):1026-35. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	1.0261 mL	5.1303 mL	10.2605 mL	25.6513 mL
	5 mM	0.2052 mL	1.0261 mL	2.0521 mL	5.1303 mL
	10 mM	0.1026 mL	0.5130 mL	1.0261 mL	2.5651 mL
	15 mM	0.0684 mL	0.3420 mL	0.6840 mL	1.7101 mL
	20 mM	0.0513 mL	0.2565 mL	0.5130 mL	1.2826 mL
	25 mM	0.0410 mL	0.2052 mL	0.4104 mL	1.0261 mL
	30 mM	0.0342 mL	0.1710 mL	0.3420 mL	0.8550 mL
	40 mM	0.0257 mL	0.1283 mL	0.2565 mL	0.6413 mL
	50 mM	0.0205 mL	0.1026 mL	0.2052 mL	0.5130 mL
	60 mM	0.0171 mL	0.0855 mL	0.1710 mL	0.4275 mL
	80 mM	0.0128 mL	0.0641 mL	0.1283 mL	0.3206 mL
	100 mM	0.0103 mL	0.0513 mL	0.1026 mL	0.2565 mL

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Navitoclax

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