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Channel Therapeutics announces efficacy results for eye drop formulations

Channel Therapeutics Corporation has achieved its predefined endpoints in two pre-clinical animal models of the Company's eye drop formulations for the treatment of both acute ocular pain as well as chronic ocular surface pain commonly associated with dry eye disease. "We are very pleased with the results of these animal efficacy studies, which adds to the Depot formulation study results announced in December 2024, demonstrating a viable path forward in treating both post-surgical pain and chronic eye pain," stated Dr. Eric Lang, Chief Medical Officer of Channel. "Additionally, these results support our belief that the inhibition of NaV1.7 has broad applications in treating different pain indications and further supports the genetic validation that NaV1.7 is a potent target for pain," concluded Dr. Lang. Trial One: In the first trial, rabbits were treated with capsaicin to mimic an acute ocular insult in a common, validated model for acute eye pain studies. Following the capsaicin treatment, the rabbits were treated with CT2000, which was dosed four times over a 24-hour period. Pain was measured by the number of paw wipes over 60 seconds. The results showed that CT2000 significantly reduced the number of paw wipes within 15 minutes of administration of capsaicin and that CT2000 continued to show efficacy over a 60-minute period following administration. This eye pain model was only validated for a short duration. Trial Two: In the second trial, benzalkonium chloride was instilled in mice eyes over a multiday period to create a model of dry eye disease. BAC is a detergent that irritates the eyes and simulates dry eye disease. As with the capsaicin model summarized above, increased paw wipes over 60 seconds were a surrogate to measure ocular pain. Following the induction of dry eye using BAC, the mice were dosed with CT2000 four times per day for 7 days. CT2000 reduced the frequency of paw wipes within a single day of administration and showed cumulative efficacy over time.

Ligand subsidiaries, Chromocell Therapeutics to merge

Ligand Pharmaceuticals (LGND) and Channel Therapeutics (CHRO) announced the signing of a definitive merger agreement to combine Ligand's wholly owned subsidiaries, Pelthos Therapeutics Inc. and LNHC, Inc. with CHRO Merger Sub Inc., a wholly owned subsidiary of Channel. The merger will be supported by $50M in capital raised from a group of strategic investors led by Murchinson. Upon completion of the transaction, the combined company will operate under the name Pelthos Therapeutics Inc. and trade on the NYSE American exchange under the ticker "PTHS." Under the terms of the merger agreement, Channel will acquire 100% of the issued and outstanding equity interests of Pelthos, and will change its name to Pelthos Therapeutics. In connection with the transaction, Ligand has agreed to invest $18M in the combined company and the Investor Group has agreed to invest $32M for a total of $50M. Upon completion of the transaction, Plesha will become CEO of the combined company and Knuettel will become CFO. The Board of Directors will consist of Plesha, two independent directors, Peter Greenleaf and Matt Pauls, two board members appointed by Ligand, and an additional two independent directors who are reasonably acceptable to Murchinson, both of whom are current Channel board members.The transaction is expected to close in the summer of 2025, subject to customary closing conditions.

Channel Therapeutics highlights difference between NaV1.7, NaV1.8

Channel Therapeutics (CHRO) is providing a statement regarding Vertex Pharmaceutical's (VRTX) recently announced Phase 2 data of Suzetrigine, an investigational, oral, highly selective NaV1.8 pain signal inhibitor in people with painful lumbosacral radiculopathy. Characteristics of Selective NaV1.7 Inhibition: NaV1.7 is a well-studied drug target with strong genetic validation - studies of inheritable pain disorders demonstrate that the spectrum of NaV1.7 activity validates the importance of this target. Lack of NaV1.7 activity leads to the inability to sense pain, whereas NaV1.7 gain of function leads to severe pain. Modulation of NaV1.7, therefore, should be an effective mechanism for decreasing pain.