Developing next-generation pharmaceuticals
One targeted mechanism.
Broad applicability in brain
dysregulation.
Clinical Proof-of-Concept
Targeting vasopressin V1a signaling across neuropsychiatric disorders and TBI.
Pathological aggression is a pervasive and highly problematic symptom. There are no targeted treatments.
Inappropriate aggression in Huntington's disease, Fragile X, and intermittent explosive disorder is managed with off-label antipsychotics and, in some cases, polypharmacy. These off-label drugs often carry safety risks and have adverse effects that impact patients, families, and caregivers. Our compounds directly address circuit abnormalites that underlie the problematic behavior without sedation or side effects. Traumatic Brain Injury, the world's most common neurological injury, has no approved drug treatments.
Vasopressin 1a (V1a) Receptor antagonism.
Circuit modulation
V1a antagonism normalizes excess AVP signaling in threat-response circuits — the substrate of pathological aggression and emotional dysregulation across CNS disorders.
Explore the scienceInjury modification
After TBI, dysregulated AVP–V1a signaling drives a signal cascade that leads to cellular damage and neuroinflammation. V1a antagonism interrupts the cascade upstream — reducing cellular damage, death, minimizing the development of post-concussion syndrome, and lowering risk for neurodegenerative disease.
How it worksClinical proof of concept
Phase 2 efficacy signal with SRX246 in pathological aggression in Hntington’s disease and Intermittent Explosive Disorder. Efficacy across two indications confirms V1a receptor as an addressable target for the management of aggression.
Pipeline statusFour programs, one shared biology — chosen where the gap is greatest.
We work where V1a signaling is well-validated, symptom burden is severe, and patients have nothing targeted today: Huntington's disease, Fragile X syndrome, intermittent explosive disorder, and mild traumatic brain injury. Success in these underserved populations opens a clear path to broader CNS conditions, including neurodegenerative diseases and additional neurodevelopmental disorders.
A genetically defined disorder with severe aggression and anxiety.
Anxiety and aggression are prominent and persistent in Fragile X syndrome — disrupting learning, social interaction, and daily life. Our DoD-funded Phase 2 study uses a double-blind crossover design with home visits to enable participation by individuals previously unable to enroll in trials. Clinical success in this rare disease should enable extension to autism spectrum disorder.
Phase 2 enrolling Q3 2026
Behavioral symptoms persist in the gene-therapy era.
Anger and aggression affect a large share of Huntington's patients and are the leading cause of institutionalization. With no approved treatments and only off-label options today, V1a antagonism offers a mechanism-based path to durable symptomatic benefit — complementary to disease-modifying therapies.
SRX246 Phase 3-ready program
An injury-modifying approach to the world's largest neurological problem.
Over 55 million TBI cases occur each year — 90% mild — with persistent post-concussion symptoms and increased risk of neurodegenerative disease. Care is largely supportive and focused on symptoms, with no approved drugs that improve neurological outcomes. Our V1a antagonists interrupt the AVP-driven secondary injury cascade upstream of edema.
SRX251 / AVN849 Phase 2a planned
Programs across neurodevelopmental, neurodegenerative, and acute indications.
One validated target — independent paths to value creation. Click into any program for current status, key readouts, and partners.