Rein Therapeutics (RNTX) investor relations material

Company Overview and Development History

• Originated as Lung Therapeutics, completed a reverse merger in October 2023, and rebranded to focus on fibrosis with a small, distributed team currently running a phase II trial in idiopathic pulmonary fibrosis (IPF).

• LTI-03, the lead drug, is a novel, first-in-class inhaled peptide that mimics caveolin-1, aiming to restore cellular homeostasis and inhibit pro-fibrotic proteins.

• The drug is delivered via a dry powder inhaler, dosed twice daily in the ongoing phase II study.

• Management team comprises experienced biotech and pulmonary leaders, with strong industry and academic backgrounds.

Mechanism of Action and Differentiation

• LTI-03 exhibits a dual mechanism: anti-fibrotic activity and preservation of type 2 alveolar epithelial cells, crucial for lung regeneration and surfactant production.

• This dual effect is unique among current IPF therapies, which primarily target fibrosis but do not protect or restore lung epithelium.

• Emphasized the rationale for using caveolin scaffolding domain peptides (CSDs) to restore homeostatic signaling lost in fibrotic diseases, supported by preclinical and clinical data.

• LTI-03’s multi-pathway approach differentiates it from approved and pipeline therapies.

Preclinical and Clinical Data Highlights

• LTI-03 demonstrated broad antifibrotic effects in vitro and in ex vivo IPF lung tissue, attenuating key profibrotic markers and restoring alveolar epithelial cell function.

• In animal models, inhaled LTI-03 reduced fibrosis, collagen deposition, and inflammatory markers, with efficacy comparable to standard-of-care drugs.

• Phase I-B trial results, published in Nature Communications, showed safety, tolerability, and positive biomarker trends, with four out of eight biomarkers reaching statistical significance.

• Exploratory biomarkers in the Phase 1b trial indicated attenuation of TSLP, IL-11, and COL1A1, consistent with preclinical findings.

• LTI-03 reduced surfactant protein D (SPD), a key biomarker linked to lung function decline, by 4.6% over two weeks.