Catalyst Pharmaceuticals Announces Filing of Patent Infringement Actions Against Jacobus Pharmaceuticals and PantherRx

Catalyst Pharmaceuticals announced that it has filed a lawsuit in the U.S. District Court for New Jersey against Jacobus Pharmaceuticals, Inc., and a lawsuit in the U.S. District Court for the Western District of Pennsylvania against PantherRx Rare LLC (PantherRx) for infringement of U.S. Patent No. 10,793,893 (the ’893 patent). The ’893 patent is exclusively licensed to Catalyst Pharmaceuticals and covers certain methods for treating disease using amifampridine drug products, including Catalyst’s Firdapse® product, in patients who are slow metabolizers of amifampridine.

The lawsuit arises from Jacobus’ and PantherRx’s sales and marketing of Ruzurgi® (amifampridine, 10 mg). The lawsuit alleges that the Ruzurgi® product infringes the ‘893 patent when administered in accordance with its product labeling. The lawsuit seeks damages and injunctive relief to prevent further marketing of Ruzurgi® in violation of Catalyst’s patent rights.

Patrick J. McEnany, Chairman and CEO of Catalyst Said: "Catalyst has invested significant resources in neuromuscular drug discovery and in building an intellectual property portfolio that aids in the discovery and development of drugs for the treatment of rare neurodegenerative diseases that are without a safe and effective FDA approved therapy, We intend to diligently and vigorously protect our patent rights for the benefit of our company and our stockholders and prevent infringing use by others. Catalyst remains confident in its patent portfolio, and has filed several additional patent applications claiming priority from the ‘893 patent to enhance the protection of the Firdapse® patent estate.”

About Firdapse®

Firdapse® (amifampridine) 10 mg tablets is an oral, nonspecific, voltage-dependent, potassium (K+) channel blocker that causes depolarization of the presynaptic membrane and slows or inhibits repolarization. This action results in the opening of slow voltage-dependent calcium (Ca2+) channels, allowing for a subsequent influx of Ca2+. In turn, it induces the exocytosis of synaptic vesicles containing Acetylcholine (ACh) to release more ACh into the synaptic cleft, enhancing neuromuscular transmission, and providing for improved muscle function.

Source: Catalyst Pharmaceuticals, Inc

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