SNV-701
Autoimmune Disease
The “oral biologic.” Multi-node immunomodulation from a single metabolic intervention. Clinical remission in treatment-resistant UC. Head-to-head ketone ester superiority over fasting. Interventional recovery in established autoimmune neurological damage.
The standard-of-care ceiling
Best-in-class biologics: 27\u201344% endoscopic remission.
The majority of IBD patients remain short of deep remission with current therapies. Secondary loss of response is endemic across all biologic classes. Each drug blocks one node; the inflammatory network reroutes.
Clinical evidence
From case remissions to mechanistic validation.
Human and preclinical evidence establishing metabolic state as a modifiable variable in autoimmune disease.
Koutsos et al., 2025 (UC + OCD remission)
Treatment-resistant ulcerative colitis patient achieved complete clinical remission with sustained metabolic intervention. Symptom improvement was inversely correlated with oscillating blood ketone levels, establishing a direct pharmacodynamic relationship: when ketones dropped, symptoms returned. When ketones were sustained, remission held.
PMID: 40248603
MS Systematic Review, 2025 (6 studies)
Consistent improvements in fatigue, depression, sleep quality, and quality of life across multiple sclerosis patients on metabolic interventions. Objective neurological gains: improved EDSS scores, walking speed, and manual dexterity. Microbiome normalization toward healthy composition.
PMID: 40951210
Saber et al., Frontiers in Immunology 2023 (Head-to-head)
Direct ketone ester (BD-AcAc2) significantly improved chronic colitis outcomes compared to intermittent fasting alone. Critical result: sustained ketone exposure, not caloric restriction, is the therapeutic driver. This eliminates the "fasting benefit" confound.
PMID: 37513865
Abdelhady et al., 2023 (Exogenous BHB)
Exogenous BHB administration inhibited NLRP3 inflammasome activation, improved colitis scores, and restored intestinal barrier function. Direct mechanistic validation: the ketone body itself mediates the anti-inflammatory effect.
PMID: 37841914
Crohn’s Disease Model, J Crohns Colitis 2026
Ketogenic intervention produced Treg expansion via the BHB axis in a Crohn’s model. Regulatory T-cell induction explains the durable remission signal: the immune system is being retrained, not just suppressed.
DOI: 10.1093/ecco-jcc/jjag003
EAE (MS model): Zyla-Jackson et al., 2023
Rapid functional improvement in motor and visual deficits when metabolic intervention was initiated after symptom onset. This is interventional, not preventive. The metabolic intervention reversed established autoimmune neurological damage.
PMID: 36937529
Mechanism of action
Seven immunomodulatory nodes. One metabolic variable.
Unlike biologics that block a single cytokine, metabolic state modulation engages multiple anti-inflammatory, barrier-restorative, and immune-regulatory pathways simultaneously.
NLRP3 inflammasome
Direct BHB-mediated inhibition of inflammasome assembly. Reduces IL-1β and IL-18, the master inflammatory cytokines driving tissue damage in IBD, MS, and autoimmune uveitis.
Youm et al., Nature Medicine 2015; Abdelhady 2023
HDAC inhibition (epigenetic)
BHB acts as an endogenous HDAC inhibitor, modulating inflammatory gene expression programs and promoting anti-inflammatory gene transcription in immune cells and epithelial tissue.
Shimazu et al., Science 2013
GPR109A/HCAR2 signaling
BHB activates the anti-inflammatory receptor GPR109A on colonic epithelium and immune cells, triggering IL-10 production and anti-inflammatory signaling cascades.
Singh et al., Immunity 2014
Regulatory T-cell expansion
Metabolic intervention promotes Treg differentiation and expansion, restoring the immunological tolerance that is lost in autoimmune conditions. Treg expansion explains the durable remission signal.
J Crohns Colitis 2026 (Crohn’s model)
Intestinal barrier restoration
BHB restores tight junction protein expression and epithelial barrier integrity, reducing the microbial translocation that drives chronic inflammatory signaling in IBD.
Abdelhady et al., 2023
Microbiome normalization
Sustained metabolic state shifts restructure the gut microbiome toward anti-inflammatory compositions, reducing pathogenic populations and expanding butyrate-producing commensals.
MS Systematic Review 2025
Microglial modulation (MS)
BHB induces anti-inflammatory ramified microglial morphology via HDAC inhibition, reducing CNS inflammation and demyelination in multiple sclerosis models.
Zyla-Jackson 2023; MCT-KD study PMID: 38054637
Development strategy
Sustained exposure is the differentiator.
The Saber 2023 head-to-head result is decisive: direct ketone ester outperformed intermittent fasting. The Koutsos 2025 case report showed symptom return when ketone levels oscillated and remission when they were sustained. The therapeutic variable is continuous metabolic state, not periodic metabolic stress.
SNV-701 is designed to deliver sustained, pharmaceutical-grade metabolic state control for autoimmune indications. Lead indications: ulcerative colitis and Crohn's disease, where the clinical and mechanistic evidence is strongest. Expansion into multiple sclerosis and autoimmune uveitis based on the growing systematic review and preclinical evidence.
The approach is orthogonal to existing biologics. SNV-701 is positioned as both a monotherapy alternative for biologic-inadequate patients and a combination partner that addresses the multi-node inflammatory architecture that single-target biologics leave partially uncontrolled.