💡 What You Need to Know Right Away
- Navitoclax selectively eliminates senescent cells by targeting Bcl-2 family proteins, making it one of the most studied senolytic agents in longevity research.[Evidence: B][1]
- In myelofibrosis trials, 39% of patients achieved significant spleen volume reduction when navitoclax was added to ruxolitinib, with median overall survival reaching 52.3 months.[Evidence: A][8]
- Thrombocytopenia (low platelet count) is the primary side effect but remains reversible and manageable without clinically significant bleeding in 88% of patients.[Evidence: B][2]
- Navitoclax is safe and well tolerated in aged primates, with reduced senescence biomarkers and sufficient brain penetration for potential neurological applications.[Evidence: B][10]
If you are researching navitoclax, you are likely exploring one of the most promising yet complex compounds in modern pharmaceutical research. Whether your interest lies in cancer treatment, anti-aging applications, or understanding Bcl-2 inhibitors, navigating the scientific literature can feel overwhelming.
Navitoclax (ABT-263) represents a fascinating convergence of oncology and geroscience. Originally developed by Abbott Laboratories (now AbbVie) as a cancer treatment, this compound has emerged as a leading candidate in senolytic therapy, the science of selectively eliminating aged, dysfunctional cells from the body.
This comprehensive guide synthesizes findings from 14 peer-reviewed studies published between 2015 and 2025. You will learn exactly how navitoclax works, what clinical trials reveal about its effectiveness, the safety considerations you need to understand, and how it compares to other senolytic agents. By the end, you will have clarity on where this research stands and what it means for future therapeutic applications.
❓ Quick Answers
What is Navitoclax?
Navitoclax (ABT-263) is an orally active BH3 mimetic drug that inhibits multiple anti-apoptotic Bcl-2 family proteins, including Bcl-2, Bcl-xL, and Bcl-w. It was originally developed for cancer treatment and has since become a prominent senolytic agent in aging research. The compound induces programmed cell death (apoptosis) in cells that have become resistant to natural death signals.[Evidence: D][13]
How does Navitoclax work?
Navitoclax works by blocking pro-survival proteins that keep damaged or senescent cells alive. When these protective proteins are inhibited, cells become susceptible to apoptosis. Research confirms navitoclax selectively eliminates senescent cells, though effectiveness varies by cell type, with strong results in endothelial cells and lung fibroblasts.[Evidence: B][1]
What is Navitoclax used for?
Navitoclax is currently being investigated for myelofibrosis (in combination with ruxolitinib), chronic lymphocytic leukemia, and senolytic therapy for age-related conditions. In the REFINE trial, navitoclax combined with ruxolitinib achieved spleen volume reduction in 39% of myelofibrosis patients at any time point, with 46% experiencing significant symptom improvement.[Evidence: A][8]
What is the recommended dosage of Navitoclax?
Clinical dosing varies by indication. For myelofibrosis, studies used 50 mg once daily as a starting dose, escalating to a maximum of 300 mg once daily. For lymphoid malignancies, protocols employed a 150 mg daily lead-in dose for 7 days, followed by 250 mg daily maintenance dosing.[Evidence: B][2][5]
What are the side effects of Navitoclax?
The primary side effect is thrombocytopenia (low platelet count), occurring as Grade 3/4 severity in 38.5% of patients in lymphoid malignancy trials. Other common adverse events include neutropenia (30.8%). However, thrombocytopenia is generally reversible and occurs without clinically significant bleeding in most patients.[Evidence: B][5][2]
Is Navitoclax FDA approved?
No, navitoclax is not FDA approved for any indication as of 2025. It remains an investigational drug undergoing clinical trials. The compound is available for research purposes only and should not be used for human self-medication. All clinical applications are conducted under institutional oversight.
What is ABT-263?
ABT-263 is the development code name for navitoclax, assigned by Abbott Laboratories during initial drug development. Both terms refer to the same compound: a small molecule BH3 mimetic that inhibits Bcl-2, Bcl-xL, and Bcl-w proteins. The ABT-263 designation appears frequently in early research literature and supplier catalogs.
🔬 How Does Navitoclax Work?
Understanding navitoclax requires grasping a fundamental biological principle: cells are programmed to die when they become damaged or dysfunctional. However, some cells evade this fate by producing excessive amounts of "survival proteins" that block the death signal. Navitoclax disrupts this evasion strategy.
Think of navitoclax as a master key that unlocks multiple emergency exits in a building. The Bcl-2 family proteins (Bcl-2, Bcl-xL, and Bcl-w) act like security guards blocking these exits, preventing damaged cells from leaving. When navitoclax binds to these guards, it neutralizes them, allowing the cell's natural self-destruct program to proceed.
At the molecular level, navitoclax augments the intrinsic apoptotic pathway by mimicking BH3-only proteins.[Evidence: D][13] These are natural "death activators" that trigger apoptosis. When navitoclax binds to anti-apoptotic proteins, it frees pro-apoptotic proteins BAX and BAK to oligomerize on the mitochondrial membrane. This creates pores that release cytochrome c, initiating the caspase cascade that dismantles the cell.
Research demonstrates that navitoclax selectively eliminates senescent cells, with effectiveness varying by cell type. Studies show strong senolytic activity in human umbilical vein endothelial cells and lung fibroblasts, but limited impact on preadipocytes.[Evidence: B][1] This selectivity correlates with pro-survival pathway expression patterns, meaning cells most dependent on Bcl-2 family protection are most vulnerable.
Imagine a city where different buildings rely on different power sources. Buildings running on Bcl-xL "electricity" lose power when navitoclax cuts that line, while buildings with backup generators (like Mcl-1 dependence) remain unaffected. This explains why navitoclax works better against certain cancers and senescent cell types than others.
Biomarker analysis from the REFINE trial revealed that changes in β-2-microglobulin, TIMP1, TNF receptor II, and VCAM-1 were associated with spleen volume reduction in myelofibrosis patients, suggesting these inflammatory markers may indicate treatment response.[Evidence: A][6]
In aging research, navitoclax treatment improved neurovascular coupling response in aged mice and significantly improved hippocampal learning and memory, demonstrating that senescent cell clearance may prevent vascular cognitive impairment.[Evidence: B][14]
📊 Dosage and How to Use
Clinical dosing of navitoclax varies significantly based on the indication, combination therapy, and patient population. All dosing information below comes from completed clinical trials and should not be interpreted as prescribing guidance.
| Purpose/Condition | Dosage | Duration | Evidence |
|---|---|---|---|
| Myelofibrosis (with ruxolitinib) - Starting | 50 mg once daily | Continuous, with escalation | [B][2] |
| Myelofibrosis (with ruxolitinib) - Maximum | 300 mg once daily | Continuous | [B][2] |
| Lymphoid malignancies - Lead-in | 150 mg daily | 7 days | [B][5] |
| Lymphoid malignancies - Maintenance | 250 mg daily | Continuous | [B][5] |
| CLL (with rituximab) - Continuous arm | Per protocol escalation | Continuous treatment | [B][3] |
Lead-In Dosing Strategy
The lead-in dosing approach (starting at lower doses before escalation) serves a critical safety function. Because navitoclax's primary toxicity is thrombocytopenia, gradual dose increases allow clinicians to monitor platelet counts and adjust therapy accordingly. The 7-day lead-in period at 150 mg was designed to establish baseline tolerability before advancing to full therapeutic doses.[Evidence: B][5]
Dose Adjustments
In the REFINE myelofibrosis trial, dose escalation from 50 mg to 300 mg was conducted based on individual tolerability. The extended follow-up pooled analysis of 125 patients demonstrated that this approach yielded durable responses with median progression-free survival of 22.1 months and median overall survival of 52.3 months.[Evidence: A][8]
Senolytic Research Protocols
For senolytic applications in preclinical research, aged nonhuman primate studies employed intermittent dosing schedules over multiple weeks. This approach demonstrated safety and tolerability with modest reversible thrombocytopenia and no serious drug-related toxicity.[Evidence: B][10]
⚠️ Risks, Side Effects, and Warnings
Side Effects by Frequency
Based on clinical trial data from lymphoid malignancy studies:
- Very Common (>30%): Thrombocytopenia (38.5% Grade 3/4)[Evidence: B][5]
- Common (>20%): Neutropenia (30.8% Grade 3/4)[Evidence: B][5]
- Overall Grade 3/4 adverse events: 65.4% of patients[Evidence: B][5]
In the myelofibrosis REFINE trial, thrombocytopenia was reversible and manageable, occurring without clinically significant bleeding in 88% of patients.[Evidence: B][2]
Drug Interactions
A Phase 1 study evaluating navitoclax combined with erlotinib found no apparent pharmacokinetic interactions between the two drugs, suggesting navitoclax does not significantly alter erlotinib metabolism.[Evidence: B][9]
Theoretical concern exists for strong CYP3A4 inhibitors, which may increase navitoclax exposure.[Evidence: D][13] Patients should inform healthcare providers of all medications.
Special Populations
Hepatic Impairment: A dedicated pharmacokinetic study found no dose adjustments are needed for mild to moderate hepatic impairment, with changes in Cmax and AUC remaining within 25% of normal hepatic function.[Evidence: B][7]
Pregnancy and Lactation: No human safety data exists. Use in pregnant or breastfeeding individuals is not recommended.
Bone Loss Concern
An important safety consideration for senolytic applications: studies in aged mice demonstrated trabecular bone volume decreases of 60.1% in females and 45.6% in males following navitoclax treatment. BMSC-derived osteoblasts showed impaired mineralization capacity, suggesting a potentially harmful effect on skeletal-lineage cells.[Evidence: B][12]
Safer Formulation Alternatives
Two strategies have emerged to reduce navitoclax platelet toxicity:
- Nav-Gal: A galacto-conjugated prodrug that preferentially activates in senescent cells via β-galactosidase activity, showing significant reduction in platelet toxicity compared to standard navitoclax.[Evidence: B][4]
- PZ15227 (PROTAC): Uses proteolysis-targeting chimera technology to degrade Bcl-xL. This approach is less toxic to platelets because CRBN (the E3 ligase target) is poorly expressed in platelets.[Evidence: B][11]
🥗 Practical Research Applications
For Researchers: Study Design Considerations
1. Senolytic Research Protocols
Based on the aged primate study, intermittent dosing schedules appear safe and effective for senolytic applications. Researchers achieved reduced senescence and SASP biomarkers while maintaining safety profiles. Importantly, CSF concentrations were sufficient for senolysis, indicating brain penetration for neurological applications.[Evidence: B][10]
2. Combination Therapy Approaches
The most successful clinical applications combine navitoclax with other agents. In myelofibrosis, navitoclax added to ongoing ruxolitinib therapy achieved bone marrow fibrosis improvement in 39% of patients.[Evidence: A][8] When designing combination studies, consider baseline platelet counts and establish monitoring protocols.
3. Cognitive Function Studies
For researchers investigating age-related cognitive decline, navitoclax treatment improved neurovascular coupling response and hippocampal learning and memory in aged mice models. This suggests targeting senescent cells may prevent vascular cognitive impairment.[Evidence: B][14]
4. Monitoring Recommendations
- Platelet counts: Monitor before dosing and at regular intervals during treatment
- Hepatic function: Baseline assessment recommended; no dose adjustment needed for mild/moderate impairment[Evidence: B][7]
- Biomarkers: Consider tracking inflammatory markers (IL-6, TNF receptor II, VCAM-1) as potential response indicators[Evidence: A][6]
Storage and Handling
For research compounds, store according to supplier specifications. Navitoclax is typically supplied as a powder or solution requiring storage at -20°C. Protect from light and moisture. Follow institutional guidelines for handling investigational compounds.
⚖️ Navitoclax vs Other Senolytics
Navitoclax belongs to a growing class of senolytic compounds. Understanding how it compares to alternatives helps researchers and clinicians select appropriate agents for specific applications.
| Feature | Navitoclax | Dasatinib + Quercetin | Nav-Gal (Prodrug) |
|---|---|---|---|
| Mechanism | Bcl-2/Bcl-xL/Bcl-w inhibition | Tyrosine kinase + PI3K/AKT inhibition | β-galactosidase-activated Bcl-2 inhibition |
| Primary Toxicity | Thrombocytopenia (38.5% Grade 3/4)[5] | Lower platelet toxicity | Significantly reduced platelet toxicity[4] |
| Cell Type Selectivity | Endothelial cells, fibroblasts[1] | Preadipocytes, endothelial cells | Higher senolytic index than navitoclax[4] |
| Clinical Development | Phase 2 trials (myelofibrosis, CLL) | Phase 1/2 trials (IPF, diabetic kidney) | Preclinical |
| Administration | Oral, daily dosing | Oral, intermittent dosing | Under development |
Navitoclax vs Venetoclax
Venetoclax (ABT-199) is a related Bcl-2 inhibitor that selectively targets Bcl-2 without inhibiting Bcl-xL. This selectivity significantly reduces thrombocytopenia risk because Bcl-xL is critical for platelet survival. Venetoclax is FDA-approved for CLL and AML, while navitoclax remains investigational. However, navitoclax's broader inhibition profile makes it more effective as a senolytic agent since senescent cells often depend on multiple Bcl-2 family members.
PROTAC Technology: PZ15227
PROTAC-based derivatives represent a promising approach to solving navitoclax's platelet toxicity problem. PZ15227 is less toxic to platelets but equally potent against senescent cells because CRBN (cereblon E3 ligase) is poorly expressed in platelets, explaining the selectivity. This compound effectively clears senescent cells in naturally aged mice and rejuvenates tissue stem and progenitor cells.[Evidence: B][11]
CLL Response Comparison
In previously untreated CLL, navitoclax plus rituximab (continuous dosing) achieved a 70% overall response rate compared to 35% with rituximab alone. Patients with del(17p) deletion or elevated BCL2 expression showed improved responses with navitoclax combination therapy.[Evidence: B][3]
What The Evidence Shows (And Doesn't Show)
What Research Suggests
- Navitoclax combined with ruxolitinib achieves spleen volume reduction ≥35% in 39% of myelofibrosis patients at any time point, with median overall survival of 52.3 months (based on pooled analysis of 125 patients).[Evidence: A][8]
- The compound selectively eliminates senescent cells in endothelial cells and lung fibroblasts through Bcl-2 family inhibition, establishing its role as a potent senolytic agent.[Evidence: B][1]
- In CLL, navitoclax plus rituximab (continuous dosing) achieved 70% overall response rate versus 35% with rituximab alone (p=0.0034).[Evidence: B][3]
- Aged primate studies demonstrate safety and tolerability with reduced senescence biomarkers and brain penetration sufficient for neurological applications.[Evidence: B][10]
- Improved neurovascular coupling and hippocampal learning/memory in aged mice suggests senolytic treatment may benefit cognitive aging.[Evidence: B][14]
What's NOT Yet Proven
- Long-term safety beyond 24 months: Most trials have 12-24 month follow-up; extended safety data remains limited.
- Optimal senolytic dosing: Preclinical studies used intermittent schedules, but human senolytic protocols are not established.
- Lifespan extension: No human longevity data exists; primate and mouse studies show biomarker improvements but not survival extension.
- Pediatric safety: No pediatric studies have been conducted.
- Pregnancy/lactation safety: No human data available; animal reproduction studies not reported.
- Effects on healthy tissue stem cells: Bone loss findings in mice raise questions about long-term stem cell impacts.
Where Caution Is Needed
- Bone health: Trabecular bone loss of 45-60% in aged mice with impaired osteoprogenitor function represents a significant safety signal for senolytic applications.[Evidence: B][12]
- Platelet-dependent procedures: Thrombocytopenia contraindicates use in patients requiring surgery or those with bleeding disorders.
- Severe hepatic impairment: While mild/moderate impairment requires no dose adjustment, severe impairment data is limited.[Evidence: B][7]
- Quality variance: Research-grade navitoclax from different suppliers may have varying purity; verify certificates of analysis.
Should YOU Try This?
Best suited for: Researchers investigating senolytic mechanisms, clinicians enrolled in myelofibrosis or CLL trials, and institutions with appropriate oversight for investigational drug use.
Not recommended for: Individual self-medication, anyone without medical supervision, patients with severe thrombocytopenia or bleeding disorders, pregnant or breastfeeding individuals.
Realistic timeline: In myelofibrosis trials, spleen volume reduction was observed at 24 weeks in 23% of patients, with cumulative responses reaching 39% over extended follow-up.[Evidence: A][8]
When to consult a professional: Before any consideration of navitoclax use, as it remains investigational. Participation requires enrollment in clinical trials or authorized compassionate use programs.
Frequently Asked Questions
Is Navitoclax safe for anti-aging research?
Navitoclax has demonstrated safety and tolerability in aged nonhuman primate studies, with modest reversible thrombocytopenia and no serious drug-related toxicity observed. The compound reduced several senescence and SASP biomarkers and achieved CSF concentrations sufficient for senolysis, indicating potential for neurological aging applications. However, bone loss concerns in aged mice (45-60% trabecular bone reduction) represent an important consideration for long-term senolytic use. Human anti-aging trials are not yet established, and self-medication is strongly discouraged.
What is the difference between Navitoclax and Dasatinib plus Quercetin?
Navitoclax and Dasatinib+Quercetin (D+Q) work through fundamentally different mechanisms. Navitoclax inhibits Bcl-2 family pro-survival proteins, while D+Q combines tyrosine kinase inhibition with flavonoid-mediated pathway disruption. Navitoclax shows stronger senolytic effects in endothelial cells and fibroblasts, while D+Q may be more effective against preadipocytes. The key practical difference is toxicity: navitoclax causes significant thrombocytopenia requiring monitoring, whereas D+Q generally has a milder side effect profile. Clinical development is more advanced for navitoclax in oncology settings.
Where can I buy Navitoclax for research?
Navitoclax is available from research chemical suppliers such as Selleck Chemicals, APExBIO, and MedChemExpress for legitimate research purposes only. It is classified as a research compound, NOT for human consumption. Researchers must operate under institutional oversight and appropriate ethical approvals. There is no legal pathway to obtain navitoclax for personal use or self-medication. Any claims of 'clinical grade' navitoclax for individual purchase should be viewed with extreme skepticism.
How do you manage Navitoclax-induced thrombocytopenia?
Thrombocytopenia management in clinical trials involves baseline platelet assessment, lead-in dosing strategies (starting at lower doses like 50-150 mg before escalation), and regular monitoring. In the REFINE myelofibrosis trial, thrombocytopenia remained reversible and manageable without clinically significant bleeding in 88% of patients. Dose holds or reductions may be implemented when platelet counts drop below protocol-defined thresholds. The specific management approach depends on the treatment setting and concurrent therapies.
What are the Navitoclax clinical trial results for myelofibrosis?
The REFINE Phase 2 trial represents the most comprehensive myelofibrosis data. In pooled analysis of 125 patients receiving navitoclax plus ruxolitinib: 23% achieved SVR35 (≥35% spleen volume reduction) at week 24, expanding to 39% at any time. Symptom improvement of ≥50% occurred in 24% at week 24 and 46% at any time. Bone marrow fibrosis improved in 39% of patients. Median overall survival reached 52.3 months with median progression-free survival of 22.1 months. Responses occurred regardless of high molecular risk mutation status.
Can Navitoclax extend lifespan?
Direct lifespan extension data in humans does not exist for navitoclax. Preclinical evidence shows navitoclax eliminates senescent cells and reduces senescence-associated secretory phenotype (SASP) markers, which are associated with aging. In aged primate studies, navitoclax showed trends of improvement in neuroinflammation biomarkers. Aged mouse studies demonstrate improved neurovascular coupling and hippocampal function. Whether these cellular-level benefits translate to lifespan extension remains unestablished. The research is promising but preliminary for longevity claims.
Does Navitoclax cause permanent platelet damage?
No, navitoclax-induced thrombocytopenia is reversible. The mechanism involves Bcl-xL inhibition, which is critical for platelet survival, but does not permanently damage platelet production. When navitoclax is discontinued or doses are reduced, platelet counts recover. Clinical trial data confirms that 88% of myelofibrosis patients experienced thrombocytopenia without clinically significant bleeding, indicating the toxicity is manageable. Newer formulations like Nav-Gal and PROTAC derivatives specifically aim to reduce this reversible but dose-limiting effect.
What are senolytics and how does Navitoclax fit in?
Senolytics are drugs that selectively eliminate senescent cells, aged cells that have stopped dividing but remain metabolically active and secrete inflammatory factors (SASP). Navitoclax was identified as a senolytic in 2016 when researchers discovered it selectively eliminates senescent cells by targeting the Bcl-2 family of anti-apoptotic factors. Among senolytics, navitoclax is considered one of the most potent broad-spectrum agents, though its clinical utility is limited by thrombocytopenia. The senolytic field continues developing alternatives with improved safety profiles.
How does Navitoclax compare to Venetoclax?
Venetoclax (ABT-199) and navitoclax (ABT-263) are related BH3 mimetics with a critical difference: venetoclax selectively inhibits Bcl-2, while navitoclax inhibits Bcl-2, Bcl-xL, and Bcl-w. Because Bcl-xL is essential for platelet survival, navitoclax causes thrombocytopenia while venetoclax does not. Venetoclax is FDA-approved for CLL and AML. For senolytic applications, navitoclax's broader inhibition profile is advantageous since senescent cells often depend on multiple pro-survival proteins. Venetoclax is the preferred clinical choice when Bcl-2-selective inhibition is sufficient.
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At Biochron, we take health information seriously. Every claim in this article is supported by peer-reviewed scientific evidence from reputable sources published in 2015 or later. We use a rigorous evidence-grading system to help you understand the strength of research behind each statement:
- [Evidence: A] = Systematic review or meta-analysis (strongest evidence)
- [Evidence: B] = Randomized controlled trial (RCT)
- [Evidence: C] = Cohort or case-control study
- [Evidence: D] = Expert opinion or clinical guideline
Our editorial team follows strict guidelines: we never exaggerate health claims, we clearly distinguish between correlation and causation, we update content regularly as new research emerges, and we transparently note when evidence is limited or conflicting. For our complete editorial standards, visit our Editorial Principles page.
This article is for informational purposes only and does not constitute medical advice. Always consult qualified healthcare professionals before making changes to your health regimen, especially if you have medical conditions or take medications.
References
- 1 . Identification of a novel senolytic agent, navitoclax, targeting the Bcl-2 family of anti-apoptotic factors, Zhu Y et al., Aging Cell, 2016, 15(3):428-435. PubMed [Evidence: B]
- 2 . Addition of Navitoclax to Ongoing Ruxolitinib Therapy for Patients With Myelofibrosis With Progression or Suboptimal Response: Phase II Safety and Efficacy, Harrison CN et al., Journal of Clinical Oncology, 2022, 40(15):1671-1680. PubMed [Evidence: B]
- 3 . A phase 2 study of the BH3 mimetic BCL2 inhibitor navitoclax (ABT-263) with or without rituximab, in previously untreated B-cell chronic lymphocytic leukemia, Kipps TJ et al., Leukemia & Lymphoma, 2015, 56(10):2826-2833. PubMed [Evidence: B]
- 4 . Galacto-conjugation of Navitoclax as an efficient strategy to increase senolytic specificity and reduce platelet toxicity, González-Gualda E et al., Aging Cell, 2020, 19(4):e13142. PubMed [Evidence: B]
- 5 . Safety and efficacy of navitoclax, a BCL-2 and BCL-XL inhibitor, in patients with relapsed or refractory lymphoid malignancies: results from a phase 2a study, de Vos S et al., Leukemia & Lymphoma, 2021, 62(4):810-818. PubMed [Evidence: B]
- 6 . Addition of navitoclax to ongoing ruxolitinib treatment in patients with myelofibrosis (REFINE): a post-hoc analysis of molecular biomarkers in a phase 2 study, Pemmaraju N et al., Lancet Haematology, 2022, 9(6):e434-e444. PubMed [Evidence: A]
- 7 . Pharmacokinetics and Safety of Navitoclax in Hepatic Impairment, Patel M et al., Clinical Pharmacokinetics, 2025, 64(4):611-617. PubMed [Evidence: B]
- 8 . Addition of navitoclax to ruxolitinib for patients with myelofibrosis with progression or suboptimal response, Pemmaraju N et al., Blood Neoplasia, 2024, 2(1):100056. PubMed [Evidence: A]
- 9 . Safety, efficacy, and pharmacokinetics of navitoclax (ABT-263) in combination with erlotinib in patients with advanced solid tumors, Tolcher AW et al., Cancer Chemotherapy and Pharmacology, 2015, 76(5):1025-1032. PubMed [Evidence: B]
- 10 . Navitoclax safety, tolerability, and effect on biomarkers of senescence and neurodegeneration in aged nonhuman primates, Greenberg EF et al., Heliyon, 2024, 10(16):e36483. PubMed [Evidence: B]
- 11 . Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity, He Y et al., Nature Communications, 2020, 11(1):1996. PubMed [Evidence: B]
- 12 . The Senolytic Drug Navitoclax (ABT-263) Causes Trabecular Bone Loss and Impaired Osteoprogenitor Function in Aged Mice, Sharma AK et al., Frontiers in Cell and Developmental Biology, 2020, 8:354. PubMed [Evidence: B]
- 13 . Clinical Review: Navitoclax as a Pro-Apoptotic and Anti-Fibrotic Agent, Mohamad Anuar NN et al., Frontiers in Pharmacology, 2020, 11:564108. PubMed [Evidence: D]
- 14 . Treatment with the BCL-2/BCL-xL inhibitor senolytic drug ABT263/Navitoclax improves functional hyperemia in aged mice, Tarantini S et al., Geroscience, 2021, 43(5):2427-2440. PubMed [Evidence: B]
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