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Antibe has identified a specialized pain indication with a significant unmet medical need for which few therapies exist. We expect to release further information about this indication once a patent application has been filed. If granted, ATB-352 will benefit from IP protection in major markets into the 2040s.
In preclinical studies, ATB-352 caused negligible gastrointestinal (“GI”) damage compared to ketoprofen alone, despite comparable suppression of intestinal prostaglandin or whole blood thromboxane synthesis.1 Rats were treated orally twice-daily for five days with either 10 mg/kg of ketoprofen, or an equimolar dose of ATB-352 of 14.5 mg/kg. (See results in accompanying graph.)
When tested over a concentration range of 3 to 30 µg/mL, no agonist effect was found against the opioid receptor, indicating that ATB-352 has no addiction potential.2
In 2020, results were published demonstrating that ATB-352 induces significantly more potent and effective analgesia than ketoprofen in a well characterized animal model of surgical pain.3 Despite the increased pain reduction, ATB-352 was much better tolerated in the GI tract; mice receiving ketoprofen exhibited a dose-dependent increase in the severity of bleeding ulcers in the stomach and intestine. In contrast, no GI damage was observed in mice treated with ATB-352, even at very high doses.3
A mechanism of action was also identified that explains the increased pain-killing effects. In addition to blocking the production of pain-promoting prostaglandins, ATB-352 further reduced pain by significantly elevating the levels of naturally-occurring endocannabinoids in comparison to the levels of endocannabinoids observed in mice treated with ketoprofen alone.3
1. Gemici et al. H2S-releasing drugs: anti-inflammatory, cytoprotective and chemopreventative potential. Nitric Oxide. 2015 Apr 30;46:25-31.
2. Antibe pre-clinical data on ATB-352.
3. Costa et al. Enhanced Analgesic Effects and GI Safety of A Novel Hydrogen Sulfide-Releasing Anti- Inflammatory Drug (ATB-352): A Role for Endogenous Cannabinoids. Antioxidant and Redox Signaling. 2020 Feb 16.