SNV-301
Serious Mental Illness
Treatment-resistant psychiatric illness shares a common metabolic signature visible on PET. 46% PANSS reduction in treatment-resistant schizophrenia. Remission documented across 7 distinct conditions. SNV-301 delivers the metabolic state that published evidence associates with psychiatric improvement, as an oral medicine.
The metabolic basis
What psychiatry calls “treatment resistance” may be a metabolic problem.
Three converging lines of evidence point to shared bioenergetic dysfunction across psychiatric diagnoses.
Glucose hypometabolism on PET
PET imaging consistently shows reduced glucose metabolism in key brain regions across schizophrenia, bipolar disorder, and major depression. The shared metabolic signature across diagnostically distinct conditions suggests a common bioenergetic substrate underlying treatment resistance.
Insulin resistance correlation
HOMA-IR was reduced by 69% in one treatment-resistant schizophrenia case during metabolic intervention. Metabolic syndrome, insulin resistance, and psychiatric treatment resistance are epidemiologically linked. The metabolic intervention addresses all three simultaneously.
Mitochondrial dysfunction markers
Postmortem and peripheral blood studies show mitochondrial complex I dysfunction, reduced ATP production, and oxidative stress across schizophrenia and bipolar disorder. Ketone bodies bypass complex I, entering the TCA cycle via succinyl-CoA.
Clinical evidence
Transdiagnostic remission data.
Published clinical outcomes from metabolic interventions across psychiatric conditions.
Danan et al., Psychiatry Research 2022 (n=31 inpatients, 6 weeks)
46% PANSS reduction (91.4 → 49.3, p<0.001) in treatment-resistant schizophrenia, schizoaffective disorder, and bipolar disorder. 27 of 27 completers improved on the Clinical Global Impression scale. This is the largest published effect in treatment-resistant psychosis from any metabolic intervention.
PMID: 35873236
Needham et al., 2024 (Case series, MDD + GAD)
Complete PHQ-9 remission in treatment-resistant major depressive disorder. GAD-7 normalization concurrent with sustained metabolic intervention. Demonstrates transdiagnostic applicability beyond psychotic spectrum.
PMID: 40083888
Laurent et al., 2025 (Schizoaffective deprescription)
Schizoaffective patient achieved stable remission with concurrent deprescription of antipsychotics during sustained metabolic intervention. Suggests metabolic state correction enables reduction of pharmacological suppression.
Lee et al., 2018 (n=15, Autism spectrum)
Significant improvement on ADOS-2 (p=0.006), the gold-standard diagnostic assessment for ASD. Metabolic intervention produced measurable improvement in core autism symptoms, not just behavioral comorbidities.
Transdiagnostic remission summary
Published clinical data now documents metabolic intervention-associated remission or significant improvement across 7 distinct psychiatric conditions: schizophrenia, bipolar disorder, MDD, schizoaffective disorder, OCD, anorexia nervosa, and autism spectrum disorder. The transdiagnostic signal is the single strongest argument for a shared metabolic substrate.
Danan 2022; Laurent 2025; Needham 2024; Lee 2018; Koutsos 2025 (OCD)
Mechanism of action
Seven validated pathways. One metabolic intervention.
Multi-pathway engagement explains the transdiagnostic signal: different conditions, same upstream metabolic deficit, same multi-node correction.
Bioenergetic restoration
Ketone bodies bypass impaired glycolysis and mitochondrial complex I, providing ATP to neurons whose glucose metabolism is compromised. FDG-PET-documented hypometabolism in psychiatric conditions represents the therapeutic target.
NLRP3 inflammasome blockade
BHB inhibits NLRP3 assembly, reducing IL-1β and IL-18. Neuroinflammation is increasingly recognized as a driver of treatment-resistant psychiatric illness. Elevated inflammatory markers predict poor response to conventional antipsychotics and antidepressants.
Youm et al., Nature Medicine 2015
GABA/glutamate rebalancing
Ketone metabolites directly inhibit vesicular glutamate transporters (VGLUT1/2), reducing excitatory neurotransmitter loading. This addresses the excitatory/inhibitory imbalance documented across schizophrenia, bipolar disorder, and epilepsy.
Juge et al., Neuron 2010
Epigenetic reprogramming
BHB acts as an endogenous HDAC inhibitor and drives lysine β-hydroxybutyrylation (Kbhb), modulating gene expression programs for BDNF (neurotrophin support), synaptic plasticity, and metabolic regulation.
Shimazu et al., Science 2013; Xie et al., Molecular Cell 2016
Insulin sensitization
Metabolic intervention reduces HOMA-IR and fasting insulin, addressing the metabolic syndrome component of psychiatric illness. Insulin resistance impairs brain glucose uptake and worsens cognitive dysfunction.
Gut-brain axis modulation
Metabolic state shifts restructure the gut microbiome, altering serotonin precursor availability, vagal afferent signaling, and systemic inflammatory tone. The microbiome-psychiatry axis is an active area of research.
BDNF upregulation
Ketone-mediated HDAC inhibition increases BDNF expression, supporting neuronal survival, synaptic plasticity, and neurogenesis. BDNF deficiency is documented across MDD, schizophrenia, and bipolar disorder.
Development strategy
The delivery problem is the opportunity.
The clinical evidence for metabolic intervention in psychiatry is striking. But the delivery vehicle (the ketogenic diet) is impractical for the population that needs it most. Psychiatric patients often struggle with basic medication adherence. Asking them to maintain an extreme diet is unrealistic. Compliance rates with the ketogenic diet in psychiatric populations are unstudied precisely because the intervention is considered impractical.
SNV-301 resolves this: an oral tablet that achieves the metabolic state associated with psychiatric improvement without dietary restriction. The pharmacological delivery of what published evidence shows works, in a form the patient population can actually use.
Lead indication: treatment-resistant bipolar depression, where the remission data is strongest and the unmet need is highest. The 505(b)(2) regulatory pathway applies. The transdiagnostic signal supports expansion across schizophrenia, MDD, OCD, and ASD with a single development platform.