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February 06, 2016 10:51 AM ET


Company Overview of Applied Genetic Technologies Corporation

Company Overview

Applied Genetic Technologies Corporation, a clinical-stage biotechnology company, develops gene therapy products to treat patients with severe inherited orphan diseases in ophthalmology in the United States. The company’s lead product candidates include treatments for X-linked retinoschisis, achromatopsia, and X-linked retinitis pigmentosa, which are inherited orphan diseases of the eye caused by mutations in single genes. It is also developing adeno-associated virus based gene therapies for the treatment of rare eye diseases; and a product candidate for treatment of alpha-1 antitrypsin deficiency for which it has conducted preclinical proof-of-concept studies and Phase I and Phase II clinic...

11801 Research Drive

Suite D

Alachua, FL 32615

United States

Founded in 1999

35 Employees



Key Executives for Applied Genetic Technologies Corporation

Chief Executive Officer, President and Director
Age: 54
Total Annual Compensation: $400.0K
Chief Financial Officer
Age: 59
Total Annual Compensation: $300.0K
Chief Medical Officer and Vice President
Age: 68
Total Annual Compensation: $350.0K
Chief Business Officer and Vice President
Age: 59
Total Annual Compensation: $127.1K
Chief Scientific Officer
Age: 55
Total Annual Compensation: $79.2K
Compensation as of Fiscal Year 2015.

Applied Genetic Technologies Corporation Key Developments

Applied Genetic Technologies Corporation - Special Call

Applied Genetic Technologies Corporation - Special Call

Applied Genetic Technologies Corporation Announces Data Evaluating Novel Aav-Based Gene Therapy as Potential Treatment for Alpha-1 Antitrypsin Deficiency

Applied Genetic Technologies Corporation announced data evaluating the use of recombinant AAV-AAT vector gene delivery to muscle in patients with alpha-1-antitrypsin (AAT) deficiency, an inherited genetic disorder that results in severe loss of lung function and is caused by complete or partial deficiency of the alpha-1 antitrypsin protein. In this study, 3 cohorts of 3 subjects each had received rAAV1-AAT by intramuscular injection at doses of 6 × 1011 (low), 1.9 × 1012 (mid), or 6 × 1012 (high) vector genomes per kilogram of body weight. Muscle biopsies at the injection site were performed at 3 months after vector injection in all 9 subjects and at 12 months after vector injection in 8 of the 9 subjects enrolled in the trial. Samples of DNA obtained from these biopsies were characterized in depth by investigators at the Children’s Hospital of Philadelphia. Each biopsy sample contained readily detectable vector DNA, the majority of which was in the form of double-stranded supercoiled and open circular episomes (segments of DNA separate from the chromosome). Episomes persisted in all participants through 12 months at only slightly lower levels than those observed at 3 months. The high copy numbers were found in a subject in the high-dose cohort, and serum AAT levels at 12 months confirmed that the high-dose group also had the high sustained serum AAT levels. Molecular clones of vector genomes derived directly from the biopsies were transcriptionally active, potentially identifying them as the source of serum AAT in the trial subjects.

Applied Genetic Technologies Corporation Announces Preclinical Data Evaluating Cone-Specific Promoters for Use in Gene Therapy of Achromatopsia and Other Retinal Diseases

Applied Genetic Technologies Corporation (AGTC) announced preclinical data evaluating cone-specific promoters for use in gene therapy of achromatopsia (ACHM) and other retinal diseases. In the study, AGTC investigators designed and constructed a series of short promoter sequences (PR1.1, PR1.5, and PR1.7) based on the 2.1 kb human L-opsin promoter. The novel short promoters were first evaluated for their efficiency and specificity in driving green fluorescent protein (GFP) expression in normal mice and cynomolgus macaques. The promoters were then tested for their ability to rescue cone function in a mouse disease model of achromatopsia associated with mutations in the CNGB3 gene. Mutations in CNGB3 are the underlying genetic cause of approximately half of achromatopsia cases in humans. When tested in mice, each of the newly designed promoters directed high expression of GFP within photoreceptors. Based on these encouraging results, a subset of the promoters was selected for study in nonhuman primates. In this study, subretinal injection of an AAV-GFP vector containing the PR1.7 promoter led to strong and specific GFP expression in all cone photoreceptor types (including L-, M-, and S- cones, corresponding to red, green, and blue cones in humans). When tested in a CNGB3 mouse mutant model of achromatopsia, subretinal injection of an AAV-CNGB3 vector containing the PR1.7 promoter rescued cone function.

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