Hoth Therapeutics’ HT-003 Inhibits Acne Gene TLR2

Initial data from the first phase of the research reports that toll-like receptor 2 (TLR2) is significantly inhibited by HT-003. 

Hoth Therapeutics, Inc. completed testing on the ability of HT-003 to block acne pathogenic gene expression in human keratinocytes.

Initial data from the first phase of the research reports that toll-like receptor 2 (TLR2) is significantly inhibited by HT-003.  In addition, HT-003 at doses as high as 50 µM led to no observable toxicity.  

Dr. Jonathan Zippin, MD, PhD, Associate Professor of Dermatology at Weill Cornell Medicine and Hoth Senior Scientific Advisor, led the first phase of the study. "Thanks to Dr. Zippin and his team, we have gained insight and gathered significant data with regards to the significance of HT-003 in blocking acne pathogenic gene expression," says Robb Knie, CEO of Hoth Therapeutics, in a news release. "We will continue to monitor the data at lower doses and move onto the testing of rodent skin and carcinogenesis."

During the next phase of the research, Dr. Zippin will identify the minimal effective dose required to block TLR2 signaling in response to a broad range of bacteria derived agonists to further elucidate the pathway.  

"The ability of HT-003 to potently inhibit TLR2 expression suggests that this drug will not only be effective for acne but may also help a broad range of patients suffering from disease driven by over active inflammatory responses to bacteria," says Dr. Zippin. 

Once HT-003 biomarkers have been identified using the in vitro human keratinocytes models, testing will move onto into live rodents.