Revolutionary Preclinical Data Unveiled by Trevena: Potential New Direction in Neuropathic Pain and Acute Seizure Management

Trevena

CHESTERBROOK, PATrevena, Inc. (Nasdaq: TRVN), announced key data today from two separate preclinical studies. The data provides fascinating insights into the potential effects of TRV045, a novel S1P1 receptor modulator, on neuropathic pain and seizure control.

Data from the first series of experiments, conducted in collaboration with scientists at Virginia Commonwealth University, demonstrated novel findings on the analgesic effects of TRV045 in animal models of chemotherapy-induced peripheral neuropathy (CIPN).

“TRV045 displayed clear and lasting analgesic-like characteristics in animal models of neuropathic pain, without evidence of peripheral lymphopenia,” affirmed Dana Selley, PhD, Professor of Pharmacology and Toxicology at Virginia Commonwealth University.

Significantly, the studies revealed that TRV045 functions differently compared to existing S1P modulators such as fingolimod, at the S1P1 receptor in CNS pain processing centers. Favorably, it neither caused receptor desensitization nor downregulation of receptor protein. These results hint that TRV045’s efficacy arises from agonist signaling.

Another striking revelation from these studies is that despite repeated dosing over 14 days, TRV045 functions differently from fingolimod, an approved S1PR modulator. Unlike fingolimod, TRV045 does not result in S1P1R functional desensitization or S1PR1 protein reduction, demonstrating its potential as a unique long-term therapeutic for neuropathic pain.

Moreover, the data indicates that TRV045 does not cause S1PR1 protein reduction or S1PR1 functional desensitization, suggesting its sustained agonism is the underlying mechanism for its analgesic effects.

The second set of studies was a separate collaboration with the NIH-supported Epilepsy Therapy Screening Program (ETSP). The recent study, featuring TRV045 in three different preclinical models, investigated its possible effects on acute seizure protection and the potential capability to modify seizure development, or epileptogenesis.

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“The data observed with TRV045 in the ETSP study program displayed a strong anticonvulsant effect across a range of animal models. Given the limited pharmacotherapy options in epilepsy, TRV045, with its unique mechanism of action, opens a significant new approach to epilepsy treatment,” stated Alexander Rotenberg, MD, PhD, Professor of Neurology at Boston Children’s Hospital and Harvard Medical School.

The outcomes of these studies align with previous data indicating TRV045 showed an anti-seizure effect in validated animal models of pharmaco-resistant epilepsy.

The ETSP plans to initiate additional studies of the anti-seizure potential of TRV045 based on these data. Even though the first assessment of the possible anti-epileptogenic effect of TRV045 did not demonstrate a statistically significant difference on the outcomes studied here, these results will guide future research and treatment considerations in seizure prevention studies.

In summary, these latest findings from Trevena are a significant contribution to current research, offering new possibilities in novel chronic pain and acute seizure management. The work continues, with additional studies to determine the potential scope of TRV045 as a revolutionary treatment.

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