Mediphron, a company researching Alzheimer's dementia treatments and non-narcotic analgesics, announced on the 17th that it has signed a contract regarding compensation for inventors of new drug substances.
A Mediphron representative explained, "This contract covers mutual cooperation for Mediphron's future development, including compensation for inventors and license-out related to the commercialization of various new drug patented substances held by Mediphron." Based on this, the company stated that it will actively pursue license-outs for its patented new drug substances.
Particularly notable is the overseas license-out of MDR-652, a non-narcotic analgesic substance (a substituted oxazole and thiazole carboxamide and urea derivative as a vanilloid receptor ligand II), for which the Clinical Study Report (CSR) for Phase 1 clinical trials was submitted to the Ministry of Food and Drug Safety in March.
MDR-652 is a potent agonist of the nociceptor known as TRPV1 and was developed targeting neuropathic pain. Phase 1 clinical trials conducted at Hallym University Sacred Heart Hospital evaluated safety, tolerability, and systemic exposure characteristics, confirming low systemic effects and excellent tolerability.
Im Jae-hong, head of Mediphron's Central Research Institute, stated, "We have reviewed various methods for the launch of MDR-652 as a new drug and are currently focusing the company's capabilities on overseas license-out as the top priority."
Meanwhile, in 2005, Mediphron signed a joint research and license-out contract worth 40 million euros (approximately 56.9 billion KRW) with German Gr?nenthal Pharma for the analgesic patented substance MDR-6013 (substituted pyrazolyl carboxamide and urea derivatives with a phenyl moiety substituted with an O-containing group as a vanilloid receptor ligand).
Additionally, Mediphron has registered a domestic patent for O-GlcNAcase (OGA) inhibitors, a lead substance for Alzheimer's dementia treatment, and is accelerating clinical research and drug development based on the beta-amyloid mechanism.
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