Announcement • May 08
Hoth Therapeutics, Inc. Secures European Authorization In Spain For HT-001 Phase 2a Trial As Interim Data Show Strong Efficacy In Cancer Patients Hoth Therapeutics, Inc. had 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 (EGFR) inhibitor therapies. Preliminary data from the ongoing study indicate: Patients achieved the primary efficacy endpoint, with rash severity reduced to clinically manageable levels (ARIGA =1) by Week 6. Over 65% of patients reported meaningful reductions in pain and itching. Zero patients required dose reduction or discontinuation of their underlying EGFR inhibitor cancer therapy. Favorable safety profile, with no treatment-limiting adverse events observed. These findings suggest that HT-001 may enable patients to remain on life-saving cancer therapies longer, addressing a major limitation of current oncology treatment regimens. The Spain authorization marks an important step in Hoth's European strategy and supports continued trial execution and expansion across additional regions. The CLEER Trial (Chemotherapy Longevity by Evading EGFR Inhibitor Reactions) is a Phase 2a randomized, placebo-controlled, parallel, dose-ranging study evaluating HT-001 in patients experiencing EGFR inhibitor-related dermatologic toxicities. HT-001 is a novel topical therapeutic designed to target inflammatory pathways associated with cancer therapy-induced skin toxicities, with the goal of improving tolerability and enabling uninterrupted treatment. Announcement • May 05
Hoth Therapeutics, Inc. Receives Nasdaq Notification of Non-Compliance with Minimum Bid Price Requirement On April 30, 2026, Hoth Therapeutics, Inc. (the Company) was notified (the Notification Letter) by The Nasdaq Stock Market, LLC (Nasdaq) that it is not in compliance with the minimum bid price requirements set forth in Nasdaq Listing Rule 5550(a)(2) for continued listing on The Nasdaq Capital Market. Nasdaq Listing Rule 5550(a)(2) requires listed securities to maintain a minimum bid price of $1.00 per share, and Nasdaq Listing Rule 5810(c)(3)(A) provides that a failure to meet the minimum bid price requirement exists if the deficiency continues for a period of 30 consecutive business days. Based on the closing bid price of the Company's common stock between March 18, 2026 and April 29, 2026, the Company no longer meets the minimum bid price requirement. The Notification Letter has no immediate effect on the listing or trading of the Company's common stock on The Nasdaq Capital Market and, at this time, the common stock will continue to trade on The Nasdaq Capital Market under the symbol HOTH. The Notification Letter provides that the Company has 180 calendar days, or until October 27, 2026, to regain compliance with Nasdaq Listing Rule 5550(a)(2). To regain compliance, the bid price of the Company's common stock must have a closing bid price of at least $1.00 per share for a minimum of 10 consecutive business days. If the Company does not regain compliance by October 27, 2026, an additional 180 days may be granted to regain compliance, so long as the Company meets The Nasdaq Capital Market continued listing requirements (except for the bid price requirement) and notifies Nasdaq in writing of its intention to cure the deficiency during the second compliance period. If the Company does not qualify for the second compliance period or fails to regain compliance during the second 180-day period, then Nasdaq will notify the Company of its determination to delist the Company's common stock, at which point the Company will have an opportunity to appeal the delisting determination to a Hearings Panel. The Company intends to monitor the closing bid price of its common stock and may, if appropriate, consider implementing available options, including, but not limited to, implementing a reverse stock split of its outstanding securities, to regain compliance with the minimum bid price requirement under the Nasdaq Listing Rules. Announcement • Apr 14
Hoth Therapeutics Reports Positive Data for GDNF in Liver Fat Metabolism and Outperforms Semaglutide Hoth Therapeutics, Inc. announced positive data from its HT-VA study, conducted under its Cooperative Research and Development Agreement (CRADA) with the U.S. Department of Veterans Affairs and Emory University, demonstrating that parenteral GDNF (Glial Cell-Derived Neurotrophic Factor) directly reprograms liver fat metabolism at the genetic level in a preclinical model of metabolic-associated fatty liver disease (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 Ppara, 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. Srebf1 reduction ? less fat being created. Ppara activation ? more fat being burned. Net effect ? reprogramming of liver metabolism. This dual mechanism suggests GDNF may offer a disease-modifying approach for MAFLD, obesity, and related metabolic disorders. The HT-VA study evaluated the effects of parenteral GDNF in a diet-induced obesity and MAFLD model. Key observations include: Western diet significantly increased liver fat accumulation and metabolic dysfunction. GDNF treatment significantly improved liver gene expression linked to fat metabolism. Reduced lipogenesis signaling (Srebf1) and enhanced metabolic regulation pathways (Ppara). Gene expression changes support improved hepatic lipid handling and metabolic efficiency. Entry into MAFLD/NASH and obesity markets. Differentiation vs. GLP-1 therapies through gene-level mechanism. Potential for first-in-class metabolic reprogramming therapy. Expansion beyond Hoth's core dermatology and oncology pipeline. Hoth plans to: Advance HT-VA findings into additional preclinical validation studies. Evaluate clinical development pathways for metabolic and liver diseases. Explore strategic partnerships and collaborations to accelerate development. 
