Dr. Richard Carliss


Assistant Professor
Biomedical Program
Office: Radford University Carilion, CRCH 810
101 Elm Avenue SE, Roanoke, VA 24013
Tel: (540) 831-1849, Fax: (540) 981-9062
E-mail: rcarliss1@radford.edu



  • BIO 211 Anatomy and Physiology
  • BIO 212 Anatomy and Physiology 
  • BIO 230, 230L Comparative Anatomy with Laboratory 
  • BIO 240, 240L Comparative Physiology with Laboratory 
  • BIO 300 Pathophysiology
  • BIO 300D Pathophysiology Online 
  • BIO 304 Genetics (3 credit) 
  • BIO 306 Genetics with Laboratory (4 credit)
  • BIO 309 Physiological Foundations of Pharmacology
  • BIO 309D Physiological Foundations of Pharmacology Online
  • BIO 311 Principles of Pharmacology
  • BIO 312 Research and Design 
  • BIO 401 Molecular Biology 
  • BIO 404 Cell Biology 
  • BIO 410 Capstone Research 
  • BIO 550D Comparative Anatomy (graduate)
  • BIOL 105 Biology for Health Science Majors



My primary project is the development of a non-opioid drug to provide new pharmaceuticals for the management of pain. With 29 years of research experience in the pharmaceutical industry, I have recently founded a start-up company called Chorda Pharma, LLC. This company is developing a novel, nonburning capsaicin for the treatment of pain. Capsaicin is the molecule in chili peppers that makes hot peppers hot. Capsaicin has been used in dozens of commercial products, as a topical pain reliever. One application can produce months of pain relief. However, the molecule also produces dermatological burning which discourages patients from its use.  

Alternatively, we have chemically modified the capsaicin molecule to a nonburning form that we will try to implement as an alternative medication to opioids for pain relief. 

A secondary research project is an ongoing analysis of telomere length in a disease state called osteogenesis imperfecta (OI).  Osteogenesis Imperfecta, or brittle bone disease, is caused by dominant mutations in specific genes directly responsible for the malformation of the collagen matrix in bone. Telomeres are the protective end caps on chromosomes that shorten with cell division and from environmental insults. If they are abnormally shortened in the DNA of OI victims, this would suggest an interaction between specifically-mutated genes in OI and the shortening dynamic associated with telomeres.  


I am using PCR to examine telomere length in Type II OI patients, where the collagen deficiency occurs in utero.  Thus cell division would be minimally affected by environmental insults.  Demonstrating that short TL is associated with Type II OI, a lethal form of OI would indicate the presence of a novel DNA regulatory pathway between COL1A1/COL1A2 genes and telomeres.