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Hoth Therapeutics mRNA Frame-Shifting Therapeutic, HT-004, Shows Potential to Reduce Lung Inflammation in Asthma and Allergy Disorders

Hoth Therapeutics mRNA Frame-Shifting Therapeutic, HT-004, Shows Potential to Reduce Lung Inflammation in Asthma and Allergy Disorders

Hoth Therapeutics, Inc. (NASDAQ: HOTH), a patient-focused biopharmaceutical company, today announced development updates for its novel asthma and allergy maintenance therapeutic, HT-004.

Hoth’s innovative approach employs a chemically-stable antisense oligonucleotide to eliminate cell surface high-affinity IgE receptor (FceRI) expression and function on mast cells and basophils, rendering mast cells unresponsive to IgE-mediated activation that occurs during asthma and allergy disorders.

Through a sponsored scientific research agreement with North Carolina State University, the team used the HT-004 FceRI mRNA frame-shifting approach to reduce lung inflammation induced by OVA in mice.  OVA-induced inflammation mice treated with HT-004 via inhalation showed significantly reduced inflammatory cell recruitment in the bronchioles compared to vehicle control and oligonucleotide control OVA-induced mice; the reduction in bronchiolar inflammation in HT-004-treated mice was near the non-OVA stimulated mice. The results of these studies support the use of HT-004 as a novel inhalation maintenance therapy for asthma and allergic disorders.

The results of these studies are a continuation of the 2016 publication by Hoth Scientific Advisory Board member Dr. Glenn Cruse, “Exon skipping of FceRIβ eliminates expression of the high-affinity IgE receptor in mast cells with therapeutic potential for allergy” (www.pnas.org/cgi/doi/10.1073/pnas.1608520113).

Hoth has filed several patent applications to protect this IP throughout the world.

Hoth is continuing to expand the HT-004 development program through investigating the therapeutic potential of HT-004 in other larger animal models (such as cats and/or dogs) that closely resemble human asthma and allergic diseases.

For more information visit Manlitics B2BTechresearchsGlobalmartek

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