LTI-03 — Clinical pipeline guide.
LTI-03 is an inhaled, first-in-class peptide derived from the scaffolding domain of Caveolin-1, a structural lung protein whose loss drives fibrotic signalling. It is Rein Therapeutics' lead clinical candidate for idiopathic pulmonary fibrosis (IPF), currently in a global Phase 2 trial.
- Seven-amino-acid peptide derived from the caveolin scaffolding domain (CSD) of Caveolin-1, delivered as an inhaled dry powder.
- Proposed dual mechanism: suppresses pro-fibrotic signalling while helping preserve alveolar epithelial type II progenitor cells needed for lung repair.
- A Phase 1b trial in 24 IPF patients (5–10 mg/day for 14 days) reported good tolerability and favourable biomarker shifts.
- Advanced into a global Phase 2 efficacy trial (RENEW, NCT06968845) in IPF patients, recruiting as of 2026.
- Developed by Rein Therapeutics (US) as a clinical drug candidate — not manufactured or sold by research-peptide vendors.
What is LTI-03?
LTI-03 is a synthetic seven-amino-acid oligopeptide built from the caveolin scaffolding domain (CSD) of Caveolin-1 (Cav-1), a structural membrane protein that helps regulate lung repair and fibrotic signalling. In idiopathic pulmonary fibrosis (IPF), Cav-1 expression falls in both lung fibroblasts and alveolar epithelial cells, and this loss is linked to the runaway scarring that defines the disease. LTI-03 is designed to replenish that missing CSD signal directly in the lung by delivering it as an inhaled, excipient-free dry powder rather than a systemic injection.
How does it work?
The peptide is thought to act on two fronts at once. First, by re-supplying CSD signalling it suppresses the profibrotic cascade that leads fibroblasts to over-produce collagen and other extracellular-matrix proteins, the material that forms lung scar tissue. Second, laboratory and ex vivo human lung-tissue studies show LTI-03 helps preserve alveolar epithelial type II (AT2) cells, the progenitor cells the lung depends on to regenerate its air-exchange surface. Modulation of collagen deposition in these lung-slice models has been reported as comparable to nintedanib, an approved IPF drug, but without triggering the apoptosis or necrosis pathways that nintedanib and pirfenidone can cause — the proposed rationale for a better tolerated, disease-modifying option.
What does the clinical evidence show?
A randomised, placebo-controlled Phase 1b study dosed 24 people with IPF with inhaled LTI-03 (5 or 10 mg/day) or placebo for 14 days. The peptide was well tolerated, with no treatment-related adverse events leading to discontinuation, and exploratory biomarker analysis from bronchial brushings suggested the drug was reaching and engaging its target cells in the lung. Those results supported the launch of a global Phase 2 efficacy trial (RENEW, NCT06968845), which began recruiting IPF patients in 2026 and is expected to report initial topline data in Q3 2026. LTI-03 does not yet have completed efficacy data in a large patient population, and it is not approved by the FDA, EMA or any other regulator.
Is LTI-03 available for research or purchase?
No. Unlike compounds such as BPC-157 or TB-500, LTI-03 is a proprietary clinical-stage drug candidate owned by Rein Therapeutics and administered only within authorised, ethics-committee-approved clinical trial sites. It is not manufactured or sold by research-peptide vendors, has no assigned CAS number in general commerce, and cannot legally or practically be sourced outside a clinical trial. PeptideCompare covers it here for scientific awareness of where inhaled peptide therapeutics for lung disease are heading, not as a sourcing guide.