About Houston Gene Therapeutics
The Mission of HGT
At Houston Gene Therapeutics, INC our history sets us apart. From the very beginnings of AAV gene therapy research, Dr. Paul Hermonat has forged a legacy of landmark research - laying the foundation for HGT today. Our mission is built upon that foundation: to develop, manufacture and deliver the safest and most effective long-term treatments (improved standard of care) to fight the major diseases of our time - including cardiovascular inflammation, aging and cancer using AAV-based gene therapy technologies.
Discovery is in Our DNA
Houston Gene Therapeutics, INC was founded by Dr. Paul Hermonat. Dr. Hermonat is a pioneer in the field AAV gene therapy, and is credited with an impressive list of groundbreaking “earliest” discoveries in the field.
A Groundbreaking Discovery
In 1983, Houston Gene Therapy CEO Dr. Paul Hermonat successfully conducted the first experiment utilizing an adeno-associated virus as a mammalian DNA cloning vector. This groundbreaking discovery continues to serve as the foundational element in AAV gene therapy today.
The photograph depicted on the cover of “Human Gene Therapy” in June of 2014 is from that original 1983 experiment. As Dr. Hermonat explains,
“It depicts the 1st AAV-based delivery of a foreign gene (NeoR, on the left) into human cells, with those transduced cells being G418 resistant. These cells could also be infected with Ad5 to rescue the AAV/NeoR DNA back out of the transduced cells. This first study shows that rAAV could deliver genes into cells, and that the rAAV could be rescued out of its integrated state by Rep expression and Ad5.”
Houston Gene Therapeutics CEO Paul Hermonat, PhD, recognized as being in the Top 2% of Impactful Researchers
Study Puts More Than 50 UAMS Faculty Among Top 2% of Influential Researchers
By: David Robinson (article is truncated)
March 16, 2022 | LITTLE ROCK — A study by Stanford University lists over 50 current and retired UAMS faculty among the top 2% of most influential researchers. The study is based on an analysis of Scopus, the largest database of peer-reviewed research literature. To determine the most influential researchers, the study authors used a combination of citation metrics to rate a researcher’s influence in their subfield over the course of their career, through 2019 – the most recently available data. Citation metrics included the h-index, a measure of a researcher’s productivity and impact; and hm-index, which accounts for the researcher’s co-authorships. The metrics were used to establish a composite indicator, or score.
The publicly available database ranks the top 100,000 researchers (out of nearly 7 million who had published at least five papers) across 22 scientific fields and 176 subfields, according to the composite citation index when self-citations were or were not included. The database also includes researchers not in the top 100,000, according to the composite index, but who were still within the top 2% of scientists in their subfield and had published at least five papers.
Internal Medicine, Cardiology
Paul L. Hermonat, Ph.D., professor, formed Houston Gene Therapeutics, Inc., retired (Cardiovascular Gene Therapy)
Jawahar L. “Jay” Mehta, M.D., Ph.D., professor (Cardiovascular Reviews)
Cam Patterson, M.D., professor (Cardiovas cular System and Hematology)
Barry Uretsky, M.D., professor* (Cardiovascular System and Hematology)
Edward T.H. Yeh, M.D., professor (Cardiovascular System and Hematology)
How we envision HGT-Cardio-1 may work in the patient with established inflammation, not only with descending aortic atherosclerosis (as shown), but with other somewhat moribund sites. Our vector may treat other sites with a high cholesterol diet induced ROS, including Ox-LDL and results in inflammation.
A high cholesterol diet induces ROS, including Ox-LDL, and results in inflammation. Ox-LDL is important ROS-inducing, inflammation-inducing.
Note that eNOX1pr is very responsive to Ox-LDL. This is exactly what we need to target/identify sites of disease and to treat them with FoxP3(p1) and IL10.
Dosage-dependent eNOX1pr expression Ox-LDL levels.
As the DNA sequence of the eNOX1pr remains stable the disappearance of Ox-LDL stimulation will result in the disappearance of eNOX1pr expression, FoxP3/IL10 treatment, as well as disease.
