Hoth Therapeutics Announces Positive Preclinical Results for HT-KIT in Aggressive Cancer Gastrointestinal Stromal Tumors (GIST). HT-KIT Triggered Significant Tumor Cell Death as Early as 24 Hours Post-treatment

In This Article:

New Data Demonstrates Significant Reduction in Tumor Growth and KIT Expression in Preclinical GIST Models

  • Induction of Tumor Cell Death – HT-KIT triggered significant tumor cell death as early as 24 hours post-treatment, while the lower dose led to delayed but substantial cell death at 72 hours.

  • Decreased Tumor Cell Proliferation – HT-KIT treatment inhibited cell growth and proliferation in GIST-T1 cells, as confirmed by cell count reductions and decreased fluorescence intensity in proliferation assays.

  • Marked Tumor Volume Reduction in GIST Mouse Models – In a humanized xenograft model, HT-KIT treatment (12.5 mg/kg IV every three days) led to a significant reduction in tumor growth, with differences becoming statistically significant by day 8 and increasing over time.

  • Consistent Tumor Size Reduction – Excised tumors from HT-KIT-treated mice were smaller and lighter than those in the control group, reinforcing tumor volume measurements.

NEW YORK, March 18, 2025 /PRNewswire/ -- Hoth Therapeutics, Inc. (NASDAQ: HOTH), a clinical-stage biopharmaceutical company, today announced breakthrough preclinical findings demonstrating the efficacy of HT-KIT, a novel targeted therapy for gastrointestinal stromal tumors (GIST). The results highlight HT-KIT's ability to significantly reduce tumor burden in humanized mouse models, disrupt KIT signaling pathways, and induce tumor cell death.

(PRNewsfoto/Hoth Therapeutics Inc.)
(PRNewsfoto/Hoth Therapeutics Inc.)

"These exciting findings mark a significant milestone in the development of HT-KIT as a potential new therapeutic for patients with GIST," said Robb Knie, CEO of Hoth Therapeutics.

"By targeting KIT mutations, which are a major driver of GIST progression, HT-KIT has shown remarkable efficacy in preclinical models, demonstrating its potential as a transformative treatment option for this difficult-to-treat cancer."

Key Findings from the Preclinical Study:

  • Significant Reduction in KIT Expression – HT-KIT effectively reduced KIT receptor expression within 24 hours, with effects sustained for 72 hours.

  • Induction of Tumor Cell Death – HT-KIT triggered significant tumor cell death as early as 24 hours post-treatment, while the lower dose led to delayed but substantial cell death at 72 hours.

  • Decreased Tumor Cell Proliferation – HT-KIT treatment inhibited cell growth and proliferation in GIST-T1 cells, as confirmed by cell count reductions and decreased fluorescence intensity in proliferation assays.

  • Marked Tumor Volume Reduction in GIST Mouse Models – In a humanized xenograft model, HT-KIT treatment led to a significant reduction in tumor growth, with differences becoming statistically significant by day 8 and increasing over time.

  • Consistent Tumor Size Reduction – Excised tumors from HT-KIT-treated mice were smaller and lighter than those in the control group, reinforcing tumor volume measurements.