Inicure

Technology

Potent agonists of the formyl peptide receptor-1 (FPR1).

Rather than attacking bacteria, Inicure harnesses the innate immune system. Our compounds selectively activate FPR1 and stimulate the NOX2 pathway, enhancing the immune system's natural production of reactive oxygen species — critical for bacterial killing and for resolving inflammation.

  1. 01

    Selective FPR1 activation

    Our small molecules act as potent, functionally selective agonists of the formyl peptide receptor-1 (FPR1) on immune cells.

  2. 02

    NOX2 and ROS response

    FPR1 signalling stimulates the NOX2 complex to produce reactive oxygen species (ROS) — a natural mechanism for bacterial killing and inflammation resolution.

  3. 03

    The immune system clears the infection

    Because the compounds do not target bacteria directly, the risk of resistance development is significantly lower.

Neutrophil engulfing a bacteria
Fig. 2 — Neutrophil engulfing a bacteria. AI generated image.

Preclinical evidence

Efficacy in human cells and preclinical models — without toxicity.

Our compounds have demonstrated efficacy against resistant pathogens including Escherichia coli (UPEC) and Staphylococcus aureus (MRSA). Because they do not directly target bacteria, the risk of resistance development is significantly lower. Early safety studies indicate no adverse toxicological effects.

Lind S, Dahlgren C, Holmdahl R, Olofsson P, Forsman H. Functional selective FPR1 signalling in favour of an activation of the neutrophil superoxide generating NOX2 complex. J Leukoc Biol. 2021; 109: 1105–1120.

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Preclinical data figure showing functional selective FPR1 signalling and NOX2 activation
Fig. 3 — FPR1 signalling and the NOX2 complex. Images by BioRender, produced by Dr Heather Chicks, Swansea University.

Academic Collaborators

  • Swansea University logo
  • Nationwide Children's logo
  • Göteborgs universitet logo

Scientific rationale for target

Why FPR1 is the right target.

  • Host-directed strategy: FPR1 is a host receptor, so activating it strengthens antibacterial immunity without adding new selection pressure on bacteria.

  • Innate immune sensing: FPR1 detects formylated bacterial peptides and primes neutrophils to recognize and attack invading pathogens.

  • Enhanced neutrophil function: FPR1 activation drives chemotaxis, phagocytosis, degranulation, and oxidative killing that clears bacterial infection.

  • Relevance to resistant infections: Because the target is the host, not the bacterium, FPR1 modulation stays effective against antibiotic-resistant pathogens.

  • Combination therapy: FPR1 modulation works alongside antibiotics: it boosts host clearance while antibiotics block bacterial growth.

FPR1 receptor signalling in a neutrophil and activation of the NOX2 complex
Fig. 4 — FPR1-mediated activation of the NOX2 pathway drives intracellular ROS production and enhanced bacterial killing.View full size

Published research

NOX2-derived ROS clear uropathogenic E. coli — and keep inflammation in check.

The study shows that reactive oxygen species generated by NADPH oxidase 2 (NOX2) — not mitochondrial ROS — drive neutrophil-mediated eradication of uropathogenic Escherichia coli (UPEC), the primary causative agent of urinary tract infection.

NOX2-derived ROS also regulate NF-κB-mediated inflammatory responses in neutrophils by releasing Nrf2 from its inhibitor Keap1. In mice lacking NOX2 (Cybb-/-), infection went uncontrolled, with heightened neutrophilic inflammation and increased bladder pathology during cystitis.

The authors conclude that neutrophil NOX2 has a dual role: eradicating UPEC while mitigating neutrophil-mediated inflammation in the urinary tract — the mechanism underpinning our NOX2-directed, host-targeted approach.

Cotzomi-Ortega I, Rosowski EE, Wang X, et al. Neutrophil NADPH oxidase promotes bacterial eradication and regulates NF-κB-mediated inflammation via NRF2 signaling during urinary tract infections. Mucosal Immunol. 2025; 18(2): 402–417.

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Schematic of a neutrophil phagocytosing uropathogenic E. coli, with NOX2-derived ROS killing bacteria and Nrf2 release limiting NF-κB-driven inflammation
Fig. 5 — Neutrophil NOX2 generates ROS that eradicate uropathogenic E. coli while Nrf2 release restrains NF-κB-mediated inflammation. Schematic illustration based on the published mechanism.

Status

Where the programme stands

  • Well-characterised, selective FPR1 agonists with single nM EC50 as lead compounds for optimisation and CD selection.

  • Patent application filed (September 2026).

  • Validated in vitro effect against several bacterial strains.

Objective and plan

Route to candidate drug selection

  1. 01

    Lead optimisation based on selected primary lead structures.

  2. 02

    ADME profiling, PK and formulation.

  3. 03

    Ex vivo target activation, selectivity and efficacy.

  4. 04

    Upscaled synthesis for preclinical in vivo models and PK.

  5. 05

    Preclinical POC in relevant infection models.

  6. 06

    CD selection and upscaled synthesis for regulatory toxicology.

Targeted patient group

Patients failed by today's antibiotics.

  • Chronic and life-threatening infections treated with suboptimal antibiotics — boosting the innate response may treat infections and save millions of patients.

  • Patients with hard-to-treat, recurrent chronic and life-threatening bacterial infections treated in hospital with anti-infective therapies, i.e. antibiotics (IV or topical).

  • Of main medical and commercial interest in high-income countries: UTI (E. coli) and infected wounds (S. aureus and P. aeruginosa).