TRV250 is being developed for the acute treatment of migraine.Learn More
Two of Trevena’s three novel drug candidates in the pipeline are being studied in close collaboration with the National Institutes of Health.
Additional pipeline assets are in development for CNS indications including migraine, opioid use disorder, and diabetic neuropathic pain.
|Program||Molecular Target||Therapeutic Target||Current Phase||PC||PH1||PH2||PH3||NDA||Approved|
|OLINVYK™ (oliceridine) injection||Mu receptor||Acute pain||Approved||Intravenous PC complete||PH1 complete||PH2 complete||PH3 complete||NDA complete||Approved in progress|
|TRV045||S1P receptor||Diabetic neuropathic pain||PH1||Oral PC complete||PH1 in progress||PH2 not started||PH3 not started||NDA not started||Approved not started|
|TRV250||Delta receptor||Acute migraine||PH1||Oral/Subcutaneous PC complete||PH1 in progress||PH2 not started||PH3 not started||NDA not started||Approved not started|
|TRV734||Mu receptor||Opioid use disorder||PH1||Oral PC complete||PH1 in progress||PH2 not started||PH3 not started||NDA not started||Approved not started|
G protein-coupled receptors (GPCRs) make up the largest family of transmembrane receptors, with approximately 34% of all U.S. Food and Drug Administration (FDA) approved drugs targeting this receptor class.
Typically, GPCR activation engages broad networks of signaling pathways, which are linked to distinct biological responses. Trevena’s compounds employ a functionally-selective MOA at the receptor site, which enables preferential activation of specific signaling pathways while minimizing activation of others.
Trevena was built from the ground up and founded on the groundbreaking work of Dr. Robert Lefkowitz out of Duke University, who later won the Nobel Prize in Chemistry for his discovery around GPCRs.
Trevena’s approach to GPCR selective agonists, which have tremendous potential for medicines that can improve patient outcomes, has yielded a set of drug candidates with the potential to engage the signaling pathways responsible for therapeutic effect, with reduced activation of the pathways responsible for adverse effects, thus allowing for a more targeted approach to delivering therapeutic benefit.