Gout Clinical Pipeline: Current Snapshot and Implications for Open Enzyme¶
Data compiled from ClinicalTrials.gov and PubMed via the Anthropic life-sciences MCP plugins on 2026-04-23. This page replaces scattered pipeline references across the wiki with a single, refreshable snapshot. Rerun the queries quarterly to keep it current — the underlying MCP calls are documented at the bottom.
Bottom line up front:
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ALLN-346 (oral gut-lumen uricase) program appears dead. The Phase 2a CKD trial was terminated September 2022 with only 19 patients enrolled against a 17-site protocol. Allena Pharmaceuticals has no active gout trials. This is a meaningful update — the wiki referenced ALLN-346 as the clinical proof-of-concept for gut-lumen uricase. The concept remains valid, but its commercial champion is gone.
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Dapansutrile (OLT1177) in gout: published Phase 2a, but no current late-phase trial. The 2020 Phase 2a proof-of-concept (N=34) showed 52–68% pain reduction at day 3 across four dose levels. Olatec's subsequent gout development appears stalled; their active programs moved to heart failure (completed) and COVID-19 (terminated). Phase 2b/3 in gout is not registered on ClinicalTrials.gov as of April 2026.
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Canakinumab finally got FDA approval for gout in August 2023 — the first biologic formally indicated for gout in the US, 12 years after its initial rejection. Our wiki references canakinumab but does not reflect this regulatory update.
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The real competitor to Open Enzyme's thesis is PRX-115 (Protalix), whose Phase 2 RELEASE trial began recruiting December 2025. It's a systemic pegylated uricase + methotrexate — same immunomodulator strategy as SEL-212/Krystexxa+MTX. PRX-115 being in Phase 2 proves the systemic-uricase-with-tolerance-induction path is alive. Open Enzyme's gut-lumen-uricase angle remains the untested and uncompeted path.
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URAT1 inhibitors are crowded. AR882 (Arthrosi), Epaminurad (JW Pharma), Dotinurad (Eisai), SAP-001 (Shanton), and ABP-671 (Atom) are all in Phase 2b/3. Competing here is not the Open Enzyme wedge.
1. Approved Therapies and Current Standard of Care¶
Source: ClinicalTrials.gov via the Anthropic life-sciences MCP; regulatory status synthesized from J Inflamm Res 2026;19 (DOI: 10.2147/JIR.S592891, PMID: 41867470).
| Therapy | Target | Status | Notes |
|---|---|---|---|
| Allopurinol | Xanthine oxidase | Generic (1966) | First-line urate-lowering; HLA-B*58:01 hypersensitivity risk |
| Febuxostat | Xanthine oxidase | Generic (2009 US) | CARES trial cardiovascular signal |
| Pegloticase (Krystexxa) | Uricase (PEGylated pig/baboon chimera) | FDA 2010 | Refractory gout only; now co-administered with methotrexate (Phase 4 NCT04772313) to mitigate anti-drug antibodies |
| Rasburicase (Elitek/Fasturtec) | Uricase (A. flavus, in S. cerevisiae) | FDA 2002 | Tumor lysis syndrome only — not approved for chronic gout. Open Enzyme's uricase is the same enzyme. |
| Lesinurad | URAT1 | FDA 2015, withdrawn 2019 | Commercial failure; Ardea Biosciences |
| Canakinumab (Ilaris) | IL-1β (mAb) | FDA approved August 2023 for gout — first biologic indication | Novartis; previously approved for CAPS/JIA. J Inflamm Res 2026 (PMID: 41867470). |
| Anakinra (Kineret) | IL-1 receptor antagonist | Off-label for gout | 2018 Sobi trial (NCT03002974) showed non-inferiority to triamcinolone |
| Rilonacept (Arcalyst) | IL-1 trap | Rejected 2012 for gout | Recent Regeneron Phase 3 (NCT00856206) in 1,315 patients — demonstrated efficacy but FDA declined |
| Colchicine | β-tubulin (CP3 ASC speck block) + P2X7 pore (CP2) | Generic | Narrow therapeutic index (~3–5×); CYP3A4/P-gp interaction surface; AGREE trial low-dose regimen; COLCOT/LoDoCo2 CV repositioning; Lodoco FDA 2023. See colchicine.md. |
| NSAIDs | COX-½ | Generic | Symptomatic only |
Implication for Open Enzyme: Pegloticase + methotrexate (Amgen/Horizon Krystexxa+MTX) and canakinumab are the "biologics" standard-of-care for refractory/hard-to-treat gout. Both are expensive and IV/SC. The oral, food-derived positioning (engineered koji as adjunct to allopurinol) avoids direct competition with these.
2. The Critical Update: ALLN-346 Program Discontinued¶
Source: NCT04987294, NCT04987242, NCT04236219, NCT05168683 via the Anthropic life-sciences ClinicalTrials.gov MCP.
Wiki references to ALLN-346 as "clinical proof-of-concept for gut-lumen uricase" are now backward-looking, not forward-looking. Status by trial:
| Trial | Phase | Status | N | Dates |
|---|---|---|---|---|
| NCT04236219 | 1 (SAD) | Completed | 24 | 2020-09 to 2020-11 |
| NCT05168683 | 1 (scintigraphy, enteric coating) | Completed | 12 | 2022-01 to 2022-02 |
| NCT04987242 | 2 (inpatient hyperuricemia) | Completed | 16 | 2021-07 to 2022-03 |
| NCT04987294 | 2a (CKD, multicenter) | TERMINATED | 19 (of planned >200 across 17 sites) | Started and terminated 2022-09-02 |
The Phase 2a CKD trial — which was the pivotal study — was terminated on its scheduled primary completion date with 19 enrolled patients across 17 US sites. No published efficacy results.
Allena Pharmaceuticals has no active trials on ClinicalTrials.gov after September 2022. The ALLN-346 asset appears to be commercially dead.
Why this matters for Open Enzyme:
- The scientific rationale for gut-lumen uricase remains intact. ABCG2-mediated gut secretion of uric acid is responsible for ~⅓ of total urate excretion (see gut-lumen-sink.md), and enzymatic degradation of luminal urate should reduce systemic load.
- The commercial proof-of-concept is absent. ALLN-346 is not a precedent for "gut-lumen uricase works in Phase 2"; it's a precedent for "one company tried this and the trial did not deliver a pivotal readout."
- This reframes Open Enzyme's positioning: we are no longer "the citizen-science version of a validated clinical program." We are "the citizen-science version of a promising mechanism that pharma has not yet validated."
- The open-source, food-grade positioning may be an advantage here — a fermented koji supplement does not need a Phase 3 trial to reach users.
Action: update the following pages to reflect ALLN-346's current status (not an endorsement, but an unfinished precedent):
- gout-deep-dive.md — "Current Treatments" section
- gut-lumen-sink.md — remove ALLN-346 as "live clinical precedent"
- engineered-yeast-uricase-proposal.md — reframe the commercial context
- index.md — "Key Science References" table (the ALLN-346 row is current truth, but should note terminated status)
Combination Positioning — Uricase Adjunct to Allopurinol (Mechanistic Extrapolation; source: ALLN-346 Study 201 enrollment criteria, above)¶
Mechanistic complementarity. Allopurinol / febuxostat inhibit xanthine oxidase (upstream urate synthesis, reduces UA production by ~60%). Engineered koji / uricase degrades UA already in the gut lumen (downstream clearance, removes urate already formed). The two do not compete — they attack different points in the urate cycle. ALLN-346's Phase 2a enrolled patients already on stable allopurinol (Study 201 in gout+CKD), explicitly positioning the enzyme as adjunct to existing therapy rather than replacement.
Why this matters for Open Enzyme. (1) Regulatory: adjunct positioning is lighter than monotherapy replacement — the enzyme is an add-on to a validated first-line, not a standalone claim. (2) Clinical: 30–40% of allopurinol-treated gout patients have imperfect UA control (above the 6 mg/dL target despite titrated allopurinol); adjunct uricase specifically addresses that residual population. (3) Self-experiment: combining engineered koji with an existing allopurinol regimen (if Brian is on one) is mechanistically additive and the safer first trial — you're adding a gut-lumen sink to an already-suppressed production rate, not removing a working drug.
Open question. Does adjunct koji allow lower allopurinol doses while maintaining target UA? A dose-sparing design is future work; first-order evidence is that adjunct reduces UA further, not that it replaces existing therapy. For HLA-B*58:01 carriers (at risk for allopurinol hypersensitivity), a successful dose-sparing result would be clinically meaningful — but proving it requires a controlled titration study that is well beyond Phase 0 scope.
See also uricase.md and engineered-koji-protocol.md.
3. The NLRP3 Inflammasome Gout Program: Dapansutrile Stalled, Pipeline Moved Elsewhere¶
According to PubMed, Dapansutrile (OLT1177) Phase 2a proof-of-concept in gout was published in Lancet Rheumatology 2020 (DOI: 10.1016/s2665-9913(20)30065-5, PMID: 33005902, Klück et al., Dinarello/Joosten groups at Radboud + Olatec).
Phase 2a results (N=34): - Open-label, 4 dose levels (100, 300, 1000, 2000 mg/day × 8 days) - Target joint pain reduction, baseline to day 3: 52.4% (100 mg), 68.4% (300 mg), 55.8% (1000 mg), 57.6% (2000 mg) — all p ≤ 0.063 - Target joint pain reduction, baseline to day 7: 82.1%, 84.2%, 68.9%, 83.9% — all p ≤ 0.031 - 25/34 patients had treatment-emergent AEs (mostly metabolism and GI); 2 SAEs (one flare worsening, one coronary stenosis unrelated) - Conclusion: "Dapansutrile is a specific NLRP3 inflammasome inhibitor with a satisfactory safety profile and efficacy in the reduction of target joint pain."
Potency reframing (ChEMBL v34 cross-check, 2026-04-23): Dapansutrile's curated cellular IC50 is 1.0 nM in mouse J774A.1 cells but 1.0 μM (1,000 nM) in human MDM cells — a 1,000× species gap (Eur J Med Chem 2020/2023; Bioorg Med Chem Lett 2021). The 100–2,000 mg/day Phase 2a oral doses are consistent with human-cell μM potency at high systemic exposure, not with sub-nanomolar MCC950-class potency. This does not diminish the Phase 2a efficacy — the clinical result stands — but it reframes how the compound class should be described to potential collaborators: dapansutrile is an oral, μM-class human NLRP3 inhibitor with a very wide mouse-vs-human potency cliff, not a sub-nanomolar miracle drug. It also validates Open Enzyme's preference for human-cell (THP-1) validation assays over rodent cellular screens. (In Vitro; source: nlrp3-inhibitor-screen.md)
What happened next: - No Phase 2b or Phase 3 in gout on ClinicalTrials.gov (as of 2026-04-23) - Olatec pivoted to heart failure (Phase 1b NCT03534297, completed 2019) and COVID-19 (Phase 2 NCT04540120, terminated 2022) - A 2026 review (J Inflamm Res, DOI: 10.2147/JIR.S592891, PMID: 41867470) describes dapansutrile as having "advanced through clinical development after incorporating safety lessons from the hepatotoxicity experience associated with MCC950" — but does not cite any pivotal gout readout beyond the 2020 paper
NLRP3 inhibitor pipeline has moved OUT of gout:
| Compound | Sponsor | Indication | Phase | Trial |
|---|---|---|---|---|
| DFV890 | Novartis | Knee osteoarthritis | 2 completed 2024-12 | NCT04886258 |
| NT-0796 | NodThera | Obesity (+ semaglutide) | 2a active 2025-10 | NCT07220629 |
| VTX3232 | Zomagen | Parkinson's | 2a completed 2025-04 | NCT06556173 |
| VENT-02 | Ventus Therapeutics | Parkinson's | 1b TERMINATED 2025-10 | NCT06822517 |
| Inzomelid | Inflazome (Roche) | CAPS (orphan) | 1 completed | NCT04015076 |
| ZYIL1 | Zydus | Healthy volunteers | 1 completed | NCT04972188 |
No active NLRP3-specific trials in gout as of April 2026. The unmet need is real (pegloticase flares during dissolution, MSU-driven pyroptosis), but the pharma interest has drifted to metabolic and neurological indications where NLRP3 biology has broader appeal.
Implication for Open Enzyme: the NLRP3 multi-target stack (oridonin + BHB + KPV + disulfiram) is not being pre-empted by a pharma success in gout. Dapansutrile's dormancy actually supports the project's "food-derived NLRP3 adjunct" positioning — the prescription pipeline isn't delivering.
Mechanistic gaps in current pipeline¶
Zileuton — the unexamined CP6a repurposing candidate. FDA-approved oral 5-LOX inhibitor for asthma (1996, generic). Direct mechanism match for CP6a (5-LOX → LTB4 → neutrophil chemotaxis — the neutrophil-amplification loop that drives gout flare pain and tissue damage). Never tested in gout — zero ClinicalTrials.gov entries as of 2026-04-24. The absence is notable given that (a) 5-LOX is as mechanistically central to gout-flare biology as COX-2 is to inflammatory pain, and (b) quercetin — a supplement with 5-LOX IC50 = 300 nM in ChEMBL — is already in the stack on this rationale. Zileuton is the pharma-grade version of a mechanism we're already trying to reach via supplements.
Cost: generic ~$50/month. Accessibility: prescription only; rheumatology or primary-care. Safety: hepatotoxicity boxed warning, monthly LFTs for first 3 months; many CYP1A2 interactions.
See wiki/zileuton.md for the full dossier including theory of mechanism, expected outcomes, comparative side-effect profile, and open questions.
4. The Direct Competitor to Watch: PRX-115 (Protalix)¶
Source: NCT07280156 via the life-sciences ClinicalTrials.gov MCP.
PRX-115 RELEASE Phase 2 trial: - Sponsor: Protalix (Karmiel, Israel — known for ProCellEx plant-cell expression platform; taliglucerase alfa precedent) - Started: 2025-12-22, primary completion 2027-12, full completion 2028-06 - N=150, multicenter Phase 2, randomized, double-blind, placebo-controlled - Intervention: Pegylated recombinant uricase, IV infusion, 24 weeks, with and without methotrexate (MTX) co-administration - Primary endpoint: % of patients with sUA <6 mg/dL for ≥80% of time during Month 6 - Key exclusion: "Prior exposure to any experimental or marketed uricase" — targeting treatment-naive gout patients - Key exclusion: eGFR ≤ 40, kidney transplant, dialysis → excludes the CKD population that ALLN-346 specifically targeted
Why this matters:
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Same strategy as SEL-212 (Sobi) and Krystexxa+MTX (Amgen): systemic uricase + immunomodulator to prevent anti-drug antibody formation. Three programs now pursuing this exact approach. The anti-drug antibody problem is real and well-characterized.
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PRX-115 is targeting the treatment-naive gout population, not just refractory/CKD. This is a more ambitious commercial positioning than pegloticase's current label.
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The gut-lumen angle is uncontested. Every competitor uses systemic delivery. None use gut-retained/lumen-active uricase. Open Enzyme's engineered koji path remains the only gut-lumen approach in any form of development, clinical or otherwise.
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Watch for RELEASE readouts. Primary completion Dec 2027 means pivotal data by Q1 2028. A positive PRX-115 readout would validate IV-uricase-with-tolerance-induction as the dominant commercial path. A negative readout would reopen the mechanism question — systemic uricase may not be tolerable long-term regardless of immunomodulation.
5. SSS11 (China): Pegylated Candida utilis Uricase¶
Source: NCT06629376 via the life-sciences ClinicalTrials.gov MCP.
- Sponsor: Shenyang Sunshine Pharmaceutical (China)
- Phase 1, N=60, recruiting since 2023, completion 2026-12
- Single center: Huashan Hospital, Fudan University, Shanghai
- Intervention: Pegylated recombinant Candida utilis uricase (PEG-CuU)
Why this is interesting to Open Enzyme:
- Candida utilis is a food-grade yeast; its uricase is one of the variants discussed in uricase-variant-selection.md alongside A. flavus (rasburicase source), A. globiformis, and B. subtilis uricases
- This is the first clinical use of a C. utilis-derived uricase
- SSS11 is still systemic IV, not gut-lumen, so it doesn't contest Open Enzyme's delivery angle
- Higher specific activity vs. A. flavus uricase is the main engineering rationale (from published biochem data); clinical-grade confirmation pending
6. Other Gout Pipeline Programs (Phase 2b / Phase 3)¶
Aggregate from the ClinicalTrials.gov MCP query: 153 total Phase ⅔ gout trials in the registry. Filtered to active or recent-pivotal programs not already covered above:
URAT1 Inhibitors (crowded field)¶
| Compound | Sponsor | Phase | Status | Trial |
|---|---|---|---|---|
| AR882 | Arthrosi Therapeutics | 3 | Active, not recruiting | NCT06846515, NCT06439602 (both 750 patients, ending 2026) |
| Epaminurad | JW Pharmaceutical | 3 | Active, not recruiting | NCT05815901 (588 patients) |
| Dotinurad | Eisai | 3 | Completed 2023-06 | NCT05007392 (451 patients vs. febuxostat) |
| SAP-001 | Shanton Pharma | 2b | Active, not recruiting | NCT05690204 (87 patients) |
| ABP-671 | Atom Therapeutics | 2 | Not yet recruiting (start 2026-06) | NCT07323095 (80 patients, CKD) |
Novel Xanthine Oxidase Inhibitors¶
| Compound | Sponsor | Phase | Status | Trial |
|---|---|---|---|---|
| Tigulixostat | LG Chem | 3 | Completed 2024-11 | NCT05586958 (354 patients) |
| HR091506 | Jiangsu Hengrui | 3 | Completed 2025-08 | NCT06139393 (765 patients) |
Uricase Programs (systemic, all IV)¶
| Compound | Sponsor | Phase | Status | Trial |
|---|---|---|---|---|
| PRX-115 | Protalix | 2 (RELEASE) | Recruiting | NCT07280156 |
| SSS11 | Shenyang Sunshine | 1 | Recruiting | NCT06629376 |
| SEL-212 | Selecta → Sobi | 3 | Completed 2022-07 | NCT04513366 (112 patients) |
| Pegloticase + MTX | Amgen (Horizon) | 4 | Completed 2022-08 | NCT04772313 |
IL-1β / Inflammasome Downstream¶
| Compound | Sponsor | Phase | Status | Trial |
|---|---|---|---|---|
| Genakumab | GeneScience (China) | 3 | Completed 2024-04 | NCT05983445 (313 patients) — Chinese canakinumab competitor |
| Anakinra vs. Prednisone in CKD gout | APHP (academic) | 2 | Suspended | NCT04844814 |
Acute Flare Novel¶
| Compound | Sponsor | Phase | Status | Trial |
|---|---|---|---|---|
| ABP-745 | Atom Therapeutics | 2 | Recruiting | NCT07145229 (380 patients, colchicine-controlled) |
6a. Acute-Flare-Abort Comparator Table — Choosing Between Options for an Active Flare (2026-05-17, source: gout-action-guide.md)¶
For recurrent-gout patients, the per-flare choice of abort therapy is a cumulative-burden decision — what you use × how many flares per year × how many decades adds up. Prednisone's per-flare burden is modest; its cumulative burden over 30 years of recurrent flares is substantial (bone loss, cataracts, adrenal suppression, glucose intolerance). The table below frames the decision across options, including anakinra SC — a cleaner IL-1R1 antagonist already in clinical use off-label for gout — and the future inhaled mRNA-IL-1RA modality.
| Option | Mechanism | Dosing for acute flare | Acute side effects | Cumulative burden (recurrent flares × decades) | Cost per flare | Access |
|---|---|---|---|---|---|---|
| Prednisone taper | Glucocorticoid receptor — system-wide | 30–40 mg/day × 5 days then taper over 7–10 days | Glucose spike, BP rise, sleep disruption, mood changes, immunosuppression | Real, dose-dependent: bone loss / osteoporosis, cataracts, adrenal suppression, glucose intolerance, weight gain | ~$10–30 (generic) | Any prescriber |
| Anakinra (Kineret) SC | IL-1R1 competitive antagonist (recombinant endogenous IL-1Ra) | 100 mg SC daily × 3 days, self-administered in thigh/abdomen | Injection-site reactions (most common); modest infection-risk signal at 3-day acute use | Minimal known burden — anakinra is recombinant version of body's endogenous IL-1Ra; no bone / glucose / adrenal effects; long-term concern is only infection masking under chronic use (not relevant for 3-day acute use × few flares/yr) | ~$300/dose × 3 = ~$900 | Rheumatologist (off-label for gout) |
| Canakinumab (Ilaris) SC | Anti-IL-1β monoclonal | 150 mg single SC | Same injection-site profile; longer half-life (~26 days) so chronic exposure window per dose | Same as anakinra's mechanism (no steroid burden); ADAs possible with chronic use but rare | ~$3,000/dose (FDA-approved for gout but cost barrier) | Rheumatologist; insurance variable |
| Colchicine + NSAID (mild flares) | Microtubule inhibition + COX | 1.2 mg colchicine + NSAID at flare onset | GI (colchicine), GI bleed risk (NSAID), renal (NSAID) | NSAID: real renal burden over years; colchicine: minimal at acute-use dose | ~$20–50 | OTC or any prescriber |
| Inhaled mRNA-IL-1RA (future, 5–10 yr horizon) | Same as anakinra — pulmonary mRNA expression of IL-1Ra | Per comp-036: BID × 4–14 days reaches median 50–56% of flare window above 80% receptor occupancy (best regimen tested); doesn't match anakinra Cmax but partial-suppression may be clinically meaningful vs prednisone burden | Pulmonary irritation; possible LNP innate immune activation; anti-PEG buildup over many lifetime exposures | TBD; in principle cleaner than steroid burden; chronic-LNP-exposure question is open | $25–200/flare projected | Doesn't exist yet (partner-tier development) |
The decision frame: if you flare 3–6× per year over decades, cumulative prednisone burden is the load-bearing concern (bone / glucose / mood / cataract effects compound). Anakinra SC is the cleanest acute-flare-abort option clinically available today — same chokepoint as canakinumab and inhaled mRNA, just SC route. Canakinumab has the longest half-life (one shot covers months) but cost is prohibitive without insurance. Colchicine + NSAID is the right tool for mild flares; inadequate for severe. The inhaled mRNA-IL-1RA route is on a 5–10 year development horizon (per comp-033 + comp-036) and is what would change the economics if it lands — same mechanism as anakinra, much lower per-dose cost, different delivery format.
Anakinra (Kineret) SC for acute flare — bridge while inhaled-mRNA pulse doesn't exist yet. Off-label for acute gout flare, used in rheumatology practice when corticosteroids are contraindicated or undesirable (recurrent flares + steroid burden). Route: subcutaneous injection in thigh or abdomen, 100 mg/day × 3 days — same SC route as insulin, the patient self-administers with a prefilled syringe. NOT intra-articular (no needle into the gout joint itself; that's a totally different procedure used for IA corticosteroid injection or the chassis-pending IA uricase concept at chassis-pending-interventions.md §6). Mechanism: recombinant IL-1 receptor antagonist (IL-1Ra) competitively blocks IL-1β signaling — aborts flare within hours via the same CP5a chokepoint as canakinumab, but daily SC dosing vs canakinumab's monthly SC + ~100× lower cost. Side-effect profile: injection-site reactions (most common), low infection-risk signal at the 3-day acute-use protocol (label cautions about TB / fungal infection are for chronic immunosuppression-tier use). Vs prednisone 30-40 mg/day × 2-week taper: anakinra is faster onset (hours vs days), narrower mechanism (single pathway block vs system-wide glucocorticoid receptor), cleaner cumulative side-effect burden over years of recurrent flares (no bone loss, no glucose intolerance, no adrenal suppression, no mood / sleep / BP effects). Cost: ~$300/dose, ~$900/flare for the 3-day protocol; insurance coverage variable for off-label use. Access: rheumatologist or forward-thinking internist willing to prescribe off-label. Bridge until the inhaled mRNA-IL-1RA modality exists (chassis-pending-interventions.md §4, 5–10 year development horizon per comp-033 partner-tier analysis); anakinra is the same mechanism + same chokepoint, just SC delivery instead of pulmonary mRNA.
Evidence level: Clinical Trial for approved indications; off-label gout use supported by the 2018 Sobi non-inferiority trial (NCT03002974) vs triamcinolone. Cumulative-burden framing is Mechanistic Extrapolation (no randomized trial comparing 30-year prednisone vs anakinra cumulative outcomes — that trial is ethically impossible and numerically intractable). (source: gout-action-guide.md)
7. Emerging Biology Worth Tracking¶
According to PubMed:
TNFSF14 as a new gout biomarker — Ea et al. Annals of the Rheumatic Diseases 2024 (DOI: 10.1136/ard-2023-225305, PMID: 38373842). Olink 92-protein inflammation panel on gout flare vs. intercritical vs. treat-to-target. TNFSF14 (TNF superfamily 14, also called LIGHT) was the highest fold-change biomarker during flare after IL-6. Ex vivo TNFSF14 blockade reduced LPS + MSU-induced cytokine response. Single-nucleotide polymorphisms in TNFSF14 affected myeloid cytokine production. This is a candidate new therapeutic target, distinct from NLRP3 and IL-1β. Not yet in any clinical program — worth tracking.
8. How to Refresh This Page¶
The data above was pulled from ClinicalTrials.gov and PubMed via the Anthropic life-sciences MCP plugins (see bio-ai-tools.md for install instructions). To regenerate a current snapshot:
ClinicalTrials.gov queries used:
search_trials(
condition="gout OR hyperuricemia",
phase=["PHASE2","PHASE3"],
status=["RECRUITING","ACTIVE_NOT_RECRUITING","NOT_YET_RECRUITING","COMPLETED"],
page_size=50
)
search_trials(intervention="dapansutrile OR OLT1177 OR NLRP3", page_size=20)
search_trials(intervention="ALLN-346 OR uricase OR rasburicase OR pegloticase",
condition="gout OR hyperuricemia", page_size=20)
search_trials(intervention="rilonacept OR canakinumab OR firsekibart OR anakinra",
condition="gout", page_size=20)
get_trial_details(nct_id=<NCT>) # for each program of interest
PubMed queries used:
search_articles(query="dapansutrile OR OLT1177 AND gout", sort="pub_date")
search_articles(query="ALLN-346 OR \"Allena Pharmaceuticals\" AND gout", sort="pub_date")
get_article_metadata(pmids=[...])
Recommended cadence: quarterly refresh. Trial statuses change (especially TERMINATED events), and new Phase ⅔ programs emerge ~1 per quarter in this therapeutic area.
Related Pages¶
- Gout Deep Dive — core pathophysiology and treatment landscape
- Gout Pathophysiology — purine metabolism, MSU crystal formation, NLRP3 activation
- Uricase — enzyme biology and evolutionary loss
- Gut-Lumen Sink — ABCG2 pathway; the insight that systemic absorption isn't needed
- NLRP3 Inflammasome — six-chokepoint model
- NLRP3 Exploit Map — multi-target stack strategy
- Engineered Yeast Uricase Proposal
- Bio-AI Tools — MCP plugin install and workflow
Generated 2026-04-23 using the Anthropic life-sciences marketplace MCP plugins (pubmed, clinical-trials). Citations include DOI links per the PubMed MCP's attribution requirement.