Science & Pipeline

The Biology of Inflammation

  1. Inflammation plays a central role in disease progression and remains an important therapeutic target across multiple indications.
  2. Patients with osteoarthritis, IPF, cardiometabolic disease and other chronic conditions face persistent unmet clinical need.
  3. The IL-6/gp130 signaling axis is a major contributor to chronic inflammation.
  4. Existing IL-6 antibodies are anti-inflammatory often acting as binary on/off switches that lead to oversuppression of immune function.
  5. A major opportunity exists for therapies that modulate—not block—IL-6/gp130 signaling to preserve beneficial pathways while reducing pathological inflammation.
Primary focus areas include Degenerative Joint Disease (DJD) / Osteoarthritis (OA), Idiopathic Pulmonary Fibrosis (IPF), and Cardiometabolic Diseases

Platform Technology

How Modulation Works

gp130 modulation technology enables customized signaling profiles across multiple disease areas driven by chronic inflammation and fibrosis

  • custom signaling profiles enabling precise tuning of 5-6 signaling pathways
  • activate and preserve beneficial STAT3
  • suppress inflammatory MAP kinase/SRC

Platform Expansion

Strategic focus on diseases of inflammation leverages gp130's central role in myeloid cell function, positioning Innata Bio to address key markets in fibrotic diseases

Modulation is Important for each Indication

Osteoarthritis (OA) - local


Clinical trial in progress NCT07308834
 

Large Unmet Need

No approved therapies that mitigate pain, improve function and halt disease progression

Validated IL-6 Biology

Proven role in cartilage degradation with differentiated local delivery approach.

Clear Regulatory Path

First-in-class opportunity with established pain and imaging endpoints

De-risked Development

Faster proof-of-concept vs. systemic indications
Idiopathic Pulmonary Fibrosis (IPF) - systemic

Myeloid Cells Drive Fibrosis

Macrophages and monocytes are central to IPF pathogenesis; gp130 is a master regulator of myeloid cell recruitment and activation

IL-6 Family Cytokines Fuel Disease

IL-6 and IL-11 mediated gp130 activation induces fibrogenic signaling and disease progression

Age-driven Innate Immune Dysfunction

IL-6 levels increase with age, impairing innate immune function

Unique First in Class Opportunity

Modulation of gp130 signaling induced by IL-6 and IL-11 targets two key fibrogenic signals with one small molecule
Cardiometabolic Diseases - systemic

Inflammation Drives Risk

IL-6 is a critical risk factor in cardiometabolic diseases, strongly correlating with mortality

IL-6 Pathway Validation

Recent late-stage clinical trials (RESCUE, Novo; POSIBIL6ESKD. CSL Behring; TRANQUILITY, Tourmaline/Novartis) have demonstrated the clinical benefit of reducing IL-6 levels in cardiometabolic diseases

Validated Biomarkers

These trials and that of Ventyx (VTX3232, NLRP3/inflammasome inhibitor) demonstrate reduced cardiometabolic risk based on serum biomarkers including IL-6, hsCRP, Lp(a) and fibrinogen

Unmet Need

Current therapies target IL-6 with mAbs. Small molecules could provide broader access