HOTH News & Events

Hoth Therapeutics announced that the U.S. Patent and Trademark Office, or USPTO, has issued a Notice of Allowance for Hoth's HT-KIT therapeutic. The allowed claims cover antisense oligomers of 25 to 50 linked nucleosides directed to splicing-relevant regions of the MS4A6A pre-mRNA, including intron 3, exon 4, and the intron 3/exon 4 junction, together with pharmaceutical compositions and methods for modulating MS4A6A mRNA splicing in cells or tissues. Hybridization of the disclosed oligomers is intended to reduce cell-surface expression of the high-affinity IgE receptor, a central driver of mast cell activation in allergic and inflammatory disease. Strategic importance includes: Allowance establishes composition-of-matter coverage for the Company's lead antisense oligomer, including modified, morpholino, and pharmaceutical composition embodiments, providing a defensible basis for the underlying chemistry of the platform; By reducing surface expression of FcRI via exon-skipping of MS4A6A pre-mRNA, the approach addresses a node upstream of histamine release and IgE-mediated degranulation, distinct from antihistamine, anti-IgE antibody, and small-molecule mast cell inhibitor approaches, Allowed method claims and related disclosures span asthma, atopic dermatitis, chronic rhinitis, allergic conjunctivitis, chronic sinusitis, anaphylaxis prevention, and mast cell-driven diseases including mastocytosis and mast cell tumors. Reinforces HT-KIT. The allowed claims strengthen the intellectual property foundation underlying HT-KIT, the Company's orphan drug-designated program for mast cell-driven disease; The application as filed also describes combination approaches with antisense oligomers targeting FcRIbeta pre-mRNA splicing, supporting future development of dual-target compositions.

Hoth Therapeutics announced that it has secured regulatory authorization in Spain for its Phase 2a CLEER trial of HT-001, while concurrently reporting encouraging interim clinical results demonstrating meaningful efficacy and safety in cancer patients experiencing EGFR inhibitor-associated skin toxicities. The authorization supports the continued advancement of Hoth's randomized, placebo-controlled, dose-ranging Phase 2a study evaluating HT-001 for the treatment of dermatologic toxicities associated with epidermal growth factor receptor inhibitor therapies.

Hoth Therapeutics announced positive data from its HT-VA study, conducted under its Cooperative Research and Development Agreement, or CRADA, with the U.S. Department of Veterans Affairs and Emory University, demonstrating that parenteral GDNF, or Glial Cell-Derived Neurotrophic Factor, directly reprograms liver fat metabolism at the genetic level in a preclinical model of metabolic-associated fatty liver disease, or MAFLD. The data highlights statistically significant improvements in key genes responsible for fat production and fat metabolism, positioning GDNF as a potentially differentiated therapeutic approach targeting the root cause of fatty liver disease and metabolic dysfunction. Statistically significant reduction in Srebf1, a key gene driving fat production in the liver: Increased expression of Pparalpha, a central regulator of fat metabolism and fat burning; GDNF outperformed semaglutide in key gene expression markers tied to liver fat regulation; Demonstrated broad metabolic impact at the genetic level, not just weight reduction. Unlike existing therapies that primarily focus on weight loss, GDNF directly targets the biological mechanisms responsible for fat accumulation in the liver. Hoth plans to: Advance HT-VA findings into additional preclinical validation studies; Evaluate clinical development pathways for metabolic and liver diseases; and explore strategic partnerships and collaborations to accelerate development.