Namodenoson Anti-Obesity Breakthrough: Can-Fite Announces Key Publication on Weight Loss Effects

Breakthrough Findings from Can-Fite's Namodenoson Study

Can-Fite BioPharma Ltd., an Israeli biotechnology firm, has unveiled a pivotal peer-reviewed publication in the International Journal of Obesity, spotlighting the anti-obesity potential of Namodenoson, their selective A3 adenosine receptor (A3AR) agonist.7828 Published on February 15, 2026, the open-access article titled "The anti-obesity effect of namodenoson, an A3 adenosine receptor agonist" details preclinical evidence showing Namodenoson curbs fat cell growth and weight gain in obesity models. This development arrives amid soaring demand for novel obesity therapies, positioning the drug as a contender in a market forecasted to exceed $60 billion by 2030.79

The study, funded by Can-Fite and involving researchers from the company's Petah-Tikva labs as well as the Liver Institute at Hadassah Medical Organization—affiliated with Hebrew University—bridges basic science and translational potential. For U.S. higher education institutions leading metabolic research, this underscores emerging pathways like A3AR modulation that could inspire collaborative studies and grant pursuits.78

Decoding the Science: What is Namodenoson and A3AR?

Namodenoson, also known as CF102, is a small-molecule oral drug that selectively activates the A3 adenosine receptor (A3AR), a G-protein-coupled receptor predominantly expressed on inflamed or diseased cells, sparing healthy ones. This selectivity contributes to its favorable safety profile, evidenced in over 1,600 patients across trials.79 Adenosine receptors, part of the purinergic signaling system, regulate inflammation, metabolism, and cell growth. While A1 and A2 subtypes have been linked to glucose handling, A3AR's role in adipogenesis—fat cell formation—is less explored but promising for obesity intervention.

In the U.S., academic labs at institutions like the University of Michigan and University of Washington have probed adenosine signaling in metabolic disorders, laying groundwork for drugs like Namodenoson. Aspiring researchers can find opportunities in higher ed research jobs focusing on receptor pharmacology.120

In Vitro Evidence: Targeting Fat Cells at the Source

The study's in vitro arm utilized 3T3-L1 pre-adipocytes, a standard murine cell line for modeling fat cell differentiation. Cells were induced to mature into adipocytes using a cocktail of dexamethasone, IBMX (3-isobutyl-1-methylxanthine), and insulin over 10-14 days. Namodenoson treatment at 5 nM and 10 nM doses inhibited proliferation by 26% and 54%, respectively (via 3H-thymidine incorporation), and reduced lipid droplet accumulation by 22% and 41% (Oil-Red-O staining).78

• Dose-dependent suppression of key adipogenic factors: PPARγ (peroxisome proliferator-activated receptor gamma), C/EBPα and β (CCAAT/enhancer-binding proteins).
• Inhibition of signaling cascades: p-AKT, PI3K, NF-κB, β-catenin.
• Upregulation of adiponectin, an anti-inflammatory hormone low in obesity.

Western blot analyses confirmed these shifts after 24-hour exposure, suggesting Namodenoson disrupts fat cell maturation at molecular levels. Such mechanistic depth appeals to U.S. university biochemists refining drug targets.

In Vivo Validation: Weight Reduction in Diet-Induced Obesity Models

Moving to whole-animal testing, C57BL/6J mice were fed a high-fat diet (60% kcal fat) for 12 weeks to induce obesity, then treated orally with 100 μg/kg Namodenoson daily for 4 weeks. Treated mice gained less weight, ending at 44.3 ± 2.2 g versus 47.2 ± 3.4 g in controls—a 6.1% difference (p=0.001). Lean-diet mice showed no change, indicating specificity to obese states.78

This mirrors prior Phase IIa MASH (metabolic dysfunction-associated steatohepatitis, formerly NASH) data where Namodenoson reduced body weight and boosted adiponectin. Phase IIb MASH trials, enrolling in the U.S., will further assess steatosis, fibrosis, and weight.37

U.S. Obesity Crisis: Why This Research Matters Now

Obesity affects 40.3% of U.S. adults, with severe cases at 9.4%, per CDC data from 2021-2023—rates holding steady into 2026 across all states.90 Annual healthcare costs top $173 billion, totaling $1.72 trillion economically.95 Comorbidities like type 2 diabetes, cardiovascular disease, and MASH strain public health systems.

Higher education plays a crucial role, training clinician-scientists and hosting NIH-funded Nutrition Obesity Research Centers (NORCs) at 11 sites including UNC Chapel Hill, UAB, UCSF, and University of Colorado Anschutz.81 These centers foster pilot grants and cores for metabolic assays, ideal for validating A3AR agonists.

Adenosine Receptor Research in American Academia

U.S. universities have pioneered adenosine studies: A2bAR work at Georgia Regents (now Augusta University) showed glucose homeostasis modulation in obesity models.119 Recent efforts at Bonn (collaborative with U.S. labs) link A2B signaling to muscle/brown fat anti-obesity effects.120 Namodenoson's A3AR focus complements this, potentially sparking cross-institutional trials.

Students and postdocs eyeing pharma-academia bridges should review academic CV tips for research fellowships.125

Namodenoson's Pipeline and Safety Edge

Beyond obesity, Namodenoson advances in Phase III hepatocellular carcinoma (HCC), Phase IIb MASH, and Phase IIa pancreatic cancer trials, with U.S. FDA Orphan and Fast Track designations.79 Unlike injectable GLP-1 agonists (e.g., semaglutide), its oral format and hepato-protective effects offer advantages, especially for liver-obesity links.

• Consistent weight loss in MASH Phase IIa: dose-dependent over 3 months.
• Broad patents cover anti-obesity use, recently expanded in U.S. and Canada.
• Low adverse events: cardio/neuro-safe.

Academic pharmacologists at clinical research jobs could contribute to upcoming expansions.

Implications for NIH-Funded University Research

NIH invests heavily in obesity via NORCs ($5-12M grants to centers like UNC's $5.6M renewal).49 Pilot programs fund A3AR-adipocyte projects, aligning with Namodenoson's adiponectin boost—key in insulin resistance.

Hadassah-Hebrew University's involvement exemplifies international ties U.S. unis like Johns Hopkins pursue in global trials. Explore research assistant positions to join such efforts.

Challenges and Future Directions in Obesity Drug Development

While promising, preclinical data requires human validation. Phase IIb MASH endpoints include weight; obesity-specific trials may follow. Challenges: translating mouse 6% reduction to humans amid GLP-1 dominance.

• Opportunities: Oral alternatives for non-responders.
• Risks: Receptor desensitization, long-term efficacy.
• Solutions: Combo therapies, university-led biomarkers.

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Stakeholder Perspectives and Broader Impacts

Pnina Fishman, Can-Fite CSO: "First evidence namodenoson targets adipocyte biology via defined pathways."79 U.S. NORC directors emphasize multi-pathway drugs for sustained loss.

Economic ripple: Reduced $173B burden frees healthcare funds. Higher ed benefits via jobs in postdoc roles and training in precision medicine.

Outlook: Paving the Way for Next-Gen Therapies

This publication catalyzes A3AR research, potentially drawing NIH R01s to U.S. labs. With obesity at 40% prevalence, innovations like Namodenoson offer hope. Researchers, advance your careers at higher ed jobs, university jobs, or career advice resources. Explore professor ratings for mentors in the field.

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