<< Back
Progress update of Vitae’s RORγt inhibitor program
  • Robust efficacy results achieved in multiple sclerosis mouse model with record-breaking speed
  • Vitae’s time from initiation of program to animal proof-of-principle with qualified lead has consistently been less than 18 months

FORT WASHINGTON, PA – June 4, 2013 – Vitae Pharmaceuticals, Inc., a clinical-stage biopharmaceutical company discovering and developing novel, small molecule, first- and bestin-class compounds, today announced that it has achieved animal proof-of-principle of one of its ROR gamma t (RORγt) inhibitor candidates in an experimental allergic encephalitis (EAE) mouse model of multiple sclerosis in only nine months, breaking the company’s previous record of 12 months. Vitae is studying its RORγt inhibitors for the treatment of a wide range of autoimmune disorders, including rheumatoid arthritis, psoriasis, steroid-resistant asthma and multiple sclerosis.

In the study, VTP-xx1 significantly reduced the severity of disease at both 10 mg/kg and 30 mg/kg oral doses. The compound demonstrated decreases in multiple cytokines/cytokine receptors in vivo, and a 50-70 percent decrease in mRNA levels of interleukin-17A (IL-17A), interleukin-17F (IL-17F) and the receptor for interleukin-23 (IL-23R). The compound was well tolerated at all doses.

“We are excited about these data as they show that Vitae’s discovery technology platform generates compounds that are safe and efficacious in a highly relevant animal model,” said Jeff Hatfield, CEO of Vitae. “Our RORγt program is a great example of Vitae’s ability to rapidly and consistently innovate against difficult targets in high-impact therapeutic categories.”

Vitae’s structure-based drug discovery approach has consistently demonstrated superior speed and performance. Time from program initiation to animal proof-of-principle with a qualified lead has been less than 18 months in each of Vitae’s programs with hard-to-drug targets. The company’s speed in its RORt program bests that of its LXR program for atherosclerosis, which achieved animal proof-of-principle in 12 months.

RORt inhibits the production of IL-17, a pro-inflammatory cytokine that is a key contributor to the pathogenesis of autoimmune inflammatory diseasessuch as psoriasis, rheumatoid arthritis, multiple sclerosis and asthma. Focusing on a small molecule solution, in just six months Vitae was able to design and synthesize compounds that solve the most critical discovery challenges including potency, isotype selectivity and PK.

“We look forward to advancing this program, which has the potential to be a first-in-class and best-in-class disease modifying agent for the treatment of autoimmune disease,” said Hatfield.

About Vitae Pharmaceuticals

Vitae Pharmaceuticals is a clinical-stage biopharmaceutical company discovering and developing a portfolio of novel, small molecule, best-in-class compounds that address important disease areas, including chronic kidney disease, diabetes, Alzheimer’s disease, and inflammation / autoimmunity.

Vitae excels at structure-based drug discovery and combines a proprietary technical platform with the insights of world class scientists to advance best-in-class compounds for high value, hard-to-drug targets. The accuracy and speed of Vitae’s drug discovery platform has enabled the company to discover and advance attractive compounds in multiple therapeutics areas in a rapid and highly capital efficient manner.

For additional information, please visit the company’s website at www.vitaepharma.com.


Tony Plohoros

"Safe Harbor" Statement under the Private Securities Litigation Reform Act of 1995: Statements in this press release regarding Vitae Pharmaceuticals Inc's business which are not historical facts are "forward-looking statements" that involve risks and uncertainties. For a discussion of such risks and uncertainties, which could cause actual results to differ from those contained in the forward-looking statements, see "Risk Factors" in the Company's Annual Report or Form 10-K for the most recently ended fiscal year.