An advancing, focused development pipeline.
Three programs targeting distinct indications where gut dysbiosis drives disease and existing therapies fall short. Each anchored in the same defined-consortium platform.
A staged development program
Three programs across distinct indications where gut dysbiosis drives disease. Filter by therapeutic area, or open any program for mechanism, status, and trial detail.
Mechanism
Antibiotics that clear C. difficile also collapse the gut's secondary-bile-acid and short-chain-fatty-acid metabolism — the very functions that keep the pathogen suppressed — leaving patients vulnerable to recurrence.5 GR-101 is a defined consortium of purified, clonally-banked Clostridia selected to reconstitute those functions: producing secondary bile acids that block C. difficile spore germination and outgrowth, and competing for the nutrients it needs to bloom.4
This is the modality and indication already validated by the first generation of defined and standardised consortia — VE303 (8 strains) cut recurrence odds by more than 80% in Phase 2, and SER-109 (VOWST) is FDA-approved — placing GR-101 on well-precedented ground.1,2 RESTORe-101, our planned Phase 1, is a randomised, double-blind, placebo-controlled study of safety, tolerability, and strain engraftment, with longitudinal bile-acid and SCFA sampling as the mechanistic readout.
Consortium composition
Representative functional classes of the GR-101 consortium. Exact isolates, ratios, and cell-bank identifiers are held as trade secret; the classes shown are anchored to published mechanism.
| Strain class | Functional role | Evidence |
|---|---|---|
| GRC-101·01 | Clostridium scindens-class — 7α-dehydroxylating | Secondary bile acids (DCA/LCA) block C. difficile germination [4] |
| GRC-101·02 | Clostridium hiranonis-class | Bile-acid 7α-dehydroxylation capacity [4] |
| GRC-101·03 | Blautia producta-class | Nutrient competition & colonisation resistance [5] |
| GRC-101·04 | Clostridium cluster IV — butyrogenic | SCFA restoration after antibiotic depletion [13] |
| GRC-101·05 | Commensal Clostridia (cluster XIVa) | Network restoration & engraftment [2] |
Mechanism
GR-201 pairs butyrate-producing commensals with Treg-inducing Clostridia to rebuild two collapsed functions of the ulcerative-colitis gut at once: short-chain-fatty-acid output and mucosal immune regulation. Butyrate directly drives differentiation of colonic Foxp3+ regulatory T cells,13,14 and a rationally selected Clostridia consortium has been shown to induce Tregs and attenuate colitis in vivo12 — the template GR-201 is built on.
Candidate strains are mined from the GutRecover library by multi-omics-guided screening against validated colitis models, benchmarked to the IBD multi-omics reference.16 The goal is to deliver the remission signal seen with donor FMT in ulcerative colitis9,10 in a defined, reproducible, manufacturable product.
Consortium composition
Representative functional classes of the GR-201 consortium, paired for butyrate output and Treg-inducing function. Exact isolates and ratios are proprietary.
| Strain class | Functional role | Evidence |
|---|---|---|
| GRC-201·01 | Faecalibacterium prausnitzii-class | Butyrate; anti-inflammatory (IL-10 / NF-κB) [15] |
| GRC-201·02 | Roseburia intestinalis-class | Butyrate production [13] |
| GRC-201·03 | Anaerostipes / Eubacterium rectale-class | Butyrogenic cross-feeding [13] |
| GRC-201·04 | Clostridia clusters IV / XIVa | Foxp3⁺ Treg induction [12] |
| GRC-201·05 | SCFA-responsive commensal | Peripheral Treg generation [23] |
Mechanism
The gut microbiome programs systemic immune tone: defined commensal consortia can deterministically expand specific T-cell populations — an 11-strain consortium elicits IFN-γ+ CD8 T cells and anti-tumour immunity in vivo.18 GR-301 applies that principle to a chronic immune-mediated condition with a consistent, replicated microbiome signature.
Discovery is gated: GR-301 advances to development-candidate nomination only once gnotobiotic colonisation establishes a causal strain→immune-phenotype link meeting a pre-defined evidence threshold. The indication is disclosed at IND.
Consortium composition
GR-301 composition is undisclosed at the discovery stage. Design follows the published precedent that a defined multi-strain consortium can deterministically program systemic T-cell phenotypes; full composition is disclosed at development-candidate nomination / IND.
| Strain class | Functional role | Evidence |
|---|---|---|
| Undisclosed | Defined consortium — CD8 / immune-tone programming | 11-strain consortium elicits IFN-γ⁺ CD8 T cells [18] |
| — | Candidate set under gnotobiotic screening | Composition disclosed at IND [20] |
No programs match these filters.
// Programs shown at their honest development stage. Every scientific claim is sourced — see Publications.