P3 Therapeutics

Pipeline

Spondyloarthritis is the lead programme

Twelve candidates, four indications, one chemistry. P3T 4.0 is the hit-to-lead candidate; the roadmap shows what has been done and what comes next.

Automated dispensing into vials (photo: National Cancer Institute, Unsplash)

Pipeline · September 2026

SpA first. Then the inflammatory diseases that share its biology.

Twelve candidates across four indications. P3T 4.0 is the hit-to-lead candidate in the spondyloarthritis programme; P3T 7.0 is in discovery and hit-to-lead optimisation for IBD. Spondyloarthritis (SpA) and inflammatory bowel disease (IBD) are deeply interconnected clinical conditions that share overlapping genetic roots, immunological pathobiology and the “gut–joint axis” — which is why the two programmes share one preclinical development path.

Indication
Candidate
Modality
Target validation
Discovery / hit-to-lead optimisation
Hit-to-lead candidate
Lead optimisation / preclinical
Lead candidate
IND enabling
Clinical
Spondyloarthritis (SpA)Lead
P3T 1.0
Small chemical molecule (SCM)
TTA
P3T 2.0
Small chemical molecule (SCM)
TTA
P3T 3.0
Small chemical molecule (SCM)
TTA
P3T 4.0
Small chemical molecule (SCM)
TTAHit-to-lead candidate
P3T 5.0
Small chemical molecule (SCM)
TTA
P3T 6.0
Molecular degrader — “glue”
ox-MIF inh.*
Inflammatory bowel disease (IBD)
P3T 7.0
Small chemical molecule (SCM)
TTA
P3T 8.0
Small chemical molecule (SCM)
TTA
Neuroinflammation (MS, Parkinson’s, Alzheimer’s)
P3T 9.0
Small chemical molecule (SCM)
TTA
P3T 10.0
Molecular degrader — PROTAC
GPX4 inh.*
Atherosclerosis
P3T 11.0
Small chemical molecule (SCM)
TTA
P3T 12.0
Small chemical molecule (SCM)
TTA

* ox-MIF and GPX4 inhibitors are degrader programmes. P3T 4.0 and P3T 7.0 have progressed through hit-to-lead optimisation into preclinical development; the remaining candidates are at target validation.

Hit-to-lead candidate

P3T 4.0 — biology assays

The hit-to-lead candidate from the spondyloarthritis programme has been profiled for absorption, distribution, metabolism and excretion (ADME), predicted human pharmacokinetics, and drug-induced liver injury (DILI) risk against a clinical reference set.

P3T 4.0 — Cell viability at 48 hours

Cell viability (luminescence) after 48 h with LPS + IFNγ stimulation: untreated and stimulated controls, vehicle, two reference drug regimens and four P3T molecules at 100 and 10 µM, three replicates each. P3T 4.0 keeps viability at the level of the stimulated control and the reference drugs at both doses.

ControlsReference drugsP3T moleculesP3T 4.0 — hit-to-lead candidatereplicates · bar = mean ± SD

Values read from the original figure (±5%); TM-1 = P3T 3.0, TM-2 = P3T 4.0, TM-4 = P3T 5.0, TM-5 = P3T 6.0 per the client. The lab should supply the raw numbers before publication.

P3T 4.0 — ADME and predicted human pharmacokinetics

Compound FKIT-T2_01-2026

ADME-ONE runs a full tier-1 ADME panel and a human PK projection on every compound, so liabilities surface early instead of late. Values with ranges are predicted human parameters; experimental inputs are measured.

PK outputs (predicted human)
Cmin,u (nM)24.1 (5.78–72.4)
Cavg,u (nM)55 (27.5–110)
Cmax,u (nM)86.1 (55.6–142)
Half-life (h)4.84 (2.78–8.97)
Bioavailability (%)72 (62.8–77.7)
CLu (mL/min/kg)76.5 (41.3–133)
Vd,u (L/kg)32.1
Experimental inputs
HLM CLint (µL/min/mg)24.5Highly favorable
MDCK Papp (×10⁻⁶ cm/s)4.63Moderate
MDCK ER1.83Moderate
Solubility (µM)80.6Moderate / good
CYP3A4 IC50 (µM)>10Highly favorable
PPB fu0.0403Challenging
Predicted inputs
LogD2.87
pKa2
Predicted human exposure — 100 mg, twice daily
Predicted human exposure×2 / ÷2 rangePredicted human Cmin,u

ADME-ONE™ — a collaboration between Inductive Bio · Ginkgo Datapoints · Tangible Scientific.

P3T 4.0 — Liver toxicity (DILI)

Lead 1 (P3T 4.0) profiled in primary human hepatocytes against Axiom’s clinical DILI reference set: imaging, transcriptomics and biochemical read-outs.

Lead candidate
951 mg
predicted toxic dose — favorable comparative liver-safety margin
MTGlo EC20
>83 µM
TV PHH nuclei loss
>83 µM
Bile-area loss
>83 µM
Morphology EC20
73.8 µM
Interpretation

No evidence of direct cytotoxicity; morphology shifts only at the highest doses tested. Hepatocyte images at 83 µM are similar to DMSO.

Clean hepatocyte imaging profile: bioactivity EC20 vs. the clinical DILI reference set
Low transcriptomic perturbation
Very low cell-viability loss

P3T 4.0 stays phenotypically quiet versus Axiom’s clinical DILI reference set.

Axiom Translate. Values read from the assay report; the lab should confirm before publication.

Roadmap

From target to launch

The standard path of a new medicine, and where P3T stands on it. Target hypothesis, target-to-hit and hit-to-lead are done; P3T 4.0 is the hit-to-lead candidate now being profiled; lead optimisation and preclinical development, lead-candidate selection and an IND filing are the next milestones.

  1. Target hypothesis Usually in academia
    May take years or decades · Triple Target Activation concept
  2. Target-to-hit ~1 year
    Identify promising compounds · in-silico screening
  3. Hit-to-lead ~1 year
    Select best compound series · 6 TTA molecules synthesised (15 pending), now in in vitro testing
  4. Hit-to-lead candidate Now
    P3T 4.0 · ADME, predicted human PK and DILI profiled · P3T 7.0 in discovery for IBD
  5. Lead optimisation / preclinical ~2 years
    Optimise potency, selectivity and ADME · in vitro and in vivo studies
  6. Lead candidate · IND ~1 year
    Lead candidate selection · IND filing (Investigational New Drug)
  7. Phase I ~1 year
    Safety in healthy volunteers
  8. Phase II ~2.5 years
    Efficacy and safety in patients
  9. Phase III ~2.5 years
    Confirm effectiveness · monitor adverse effects
  10. Submission to launch ~1.5 years
    Regulatory review · approval process

Investors

Ready to invest?

P3T is raising a €1M seed round to biological proof of concept. Download the pitch deck or get in touch.