Purine, Meet Your Match: How Streptococcus thermophilus IDCC 2201 Lowers Uric Acid

A purine-degrading probiotic with in-vivo efficacy—and what it means for anti-hyperuricemia product design

Rising hyperuricemia—and the gout risk that follows—has brands searching beyond xanthine-oxidase inhibitors and “low-purine” claims. A 2024 PLOS ONE study spotlights a different angle: degrading purine nucleosides upstream and nudging the gut ecosystem toward short-chain-fatty-acid (SCFA) recovery. The hero strain is Streptococcus thermophilus IDCC 2201, developed in Korea. Below is a concise, data-first readout for B2B formulators.

Mechanism First: Purine Salvage, Not Just Inhibition

HGPRT on board, hypoxanthine and inosine broken down

• Genomics: IDCC 2201 carries hpt/HGPRT (locus_tag = ESP48_05170), enabling purine salvage (hypoxanthine/guanine → IMP/GMP), a route that reduces substrates feeding uric acid.

• In-vitro degradation (1.25 mM, HPLC, 1 h):

  • Hypoxanthine: 48.48 ± 0.04% degraded (IDCC 2201)

  • Inosine: 50.12% degraded (IDCC 2201)

  • Comparators (inosine): L. plantarum CR1 84.65%, L. pentosus GZ1 99.98%

  • Comparators (hypoxanthine): CR1 1.42 ± 2.05%, GZ1 0.69 ± 1.13%(Key take: IDCC 2201 targets hypoxanthine especially well—strategically relevant because hypoxanthine sits just one step upstream of uric acid.) 

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Study Design at a Glance

SD rats, PO-induced hyperuricemia, 7-day oral dosing

• Model: Sprague–Dawley rats; hyperuricemia induced with potassium oxonate (PO) for 7 days.

• Arms (N=6/group): Normal (G1), HU control (G2), CR1 (G3), GZ1 (G4), IDCC 2201 1×10⁸ CFU/day (G5), CR1+IDCC 2201 (G6), GZ1+IDCC 2201 (G7), L. gasseri PA-3 (G8), Allopurinol 50 mg/kg (G9).

• Model check: G2 serum UA 2.97 ± 1.01 mg/dL vs G1 1.17 ± 0.15 mg/dL (↑, p<0.001).

  
  

Primary Efficacy: Serum Uric Acid (SUA)

IDCC 2201 alone and in a combo both moved the needle

• Monotherapy (G5, 1×10⁸ CFU/day): SUA ↓ 1.48 ± 0.65 mg/dL vs HU control (p<0.05).

  • Paper-reported relative change: −50.11% vs G2.

• Combo (G6, CR1+IDCC 2201): SUA ↓ 1.80 ± 0.50 mg/dL vs HU control (p<0.05).

  • Paper-reported relative change: −39.33% vs G2.

• Context: Reported effects compare favorably with prior LAB data (e.g., L. fermentum NCUH003018 ~30.77%).

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Dose–Response & Reproducibility

High dose (1×10⁹ CFU/day) confirmed effect in a second cohort

A separate, dose-ranging study (N=8/group) tested 1×10⁹, 1×10⁸, 1×10⁷ CFU/day of IDCC 2201 for 7 days:

• G2 (HU control): 1.61 ± 0.42 mg/dL

• IDCC 2201 1×10⁹ (G3): 1.18 ± 0.26 mg/dL (p<0.05 vs G2)

• IDCC 2201 1×10⁸ (G4): 1.45 ± 0.45 mg/dL (ns)

• IDCC 2201 1×10⁷ (G5): 1.38 ± 0.63 mg/dL (ns)Takeaway: Efficacy reproduced at the high dose; mid/low doses trended but were not significant in this short course.

  
  

Microbiome & Metabolites

SCFAs recovered; butyrate-linked taxa increased

• SCFAs (fecal): HU lowered acetate and butyrate vs normal; IDCC 2201 (1×10⁹) significantly increased both vs HU (both p<0.001).

• Taxa shifts (LEfSe): ↑ Lachnospiraceae (LDA = 5.059; p = 0.002), ↑ Blautia (LDA = 3.798; p = 0.036), ↑ Roseburia (LDA = 3.537; p = 0.010), ↑ Bacteroides acidifaciens (LDA = 3.564; p = 0.034); all supportive of butyrate production and barrier integrity.

  
  

What This Means for Product Strategy

A differentiated claim architecture for anti-hyperuricemia concepts

• Positioning: “Purine-nucleoside degradation” (upstream of uric acid) + “microbiome/SCFA restoration” offers a distinct story from classical XO-inhibition.

• Formats & doses: Evidence favors ≥1×10⁹ CFU/day for short-course impact in vivo; build headroom for real-world adherence and matrix losses.

• Regulatory reality check: Today’s data are preclinical; human trials will be required before disease-risk reduction claims. Keep language to “supports healthy uric acid metabolism” and “helps manage dietary purine load” where appropriate.

Quick Data Sheet

Key numbers at a glance

• Gene/Mechanism: hpt/HGPRT present (purine salvage).

• In-vitro (1 h): Hypoxanthine 48.48 ± 0.04%; Inosine 50.12% (IDCC 2201). Comparators (inosine): CR1 84.65%, GZ1 99.98%. Comparators (hypoxanthine): CR1 1.42 ± 2.05%, GZ1 0.69 ± 1.13%.

• In-vivo (N=6): HU control 2.97 ± 1.01 mg/dL vs normal 1.17 ± 0.15; IDCC 2201 −1.48 ± 0.65 mg/dL; Combo (CR1+IDCC 2201) −1.80 ± 0.50 mg/dL (both p<0.05).

• Dose study (N=8): IDCC 2201 1×10⁹ → 1.18 ± 0.26 mg/dL vs HU 1.61 ± 0.42 (p<0.05). 1×10⁸ and 1×10⁷ not significant.

• Microbiome/SCFAs: ↑ acetate, ↑ butyrate (both p<0.001); ↑ Lachnospiraceae, Blautia, Roseburia, B. acidifaciens.

Final Thoughts: Redefining Uric Acid Management Through the Microbiome

The findings on Streptococcus thermophilus IDCC 2201 open a new frontier in uric acid management—one that targets purine metabolism upstream while simultaneously restoring gut-derived SCFAs and beneficial taxa. This dual-action mechanism differentiates it from conventional xanthine-oxidase inhibitors, offering a science-backed pathway for developing next-generation supplements aimed at supporting healthy uric acid levels. While human clinical validation will be the next crucial step, the data position IDCC 2201 as a promising candidate for innovative, microbiome-centered approaches to hyperuricemia.