Resolving fibrosis at its cellular source.

Fibrosis is a convergent, organ-agnostic pathology driven by persistent myofibroblast activation and dysregulated extracellular-matrix remodeling. We develop precision therapeutics directed at the activated stromal compartment.

~18%
of global deaths involve fibrosis, and rising (GBD 2019)
Organ-agnostic
cardiac, pulmonary, hepatic, renal & dermal
Few
disease-modifying antifibrotics; none curative
The science

A self-sustaining fibrogenic program underlies organ failure.

Across tissues, chronic injury and inflammatory signaling drive the trans-differentiation of resident fibroblasts into activated myofibroblasts. These cells deposit and crosslink extracellular matrix, stiffen the parenchyma, and reinforce their own activation through paracrine feedback — producing progressive, frequently irreversible loss of organ function.

Injury & inflammatory cues

Sustained tissue stress and pro-fibrotic cytokine signaling prime the stromal niche.

Myofibroblast activation

Resident fibroblasts adopt a contractile, matrix-secreting phenotype and remodel the ECM.

Matrix accumulation & stiffening

Crosslinked collagen and mechano-feedback perpetuate activation, driving organ dysfunction.

Our approach

Selectivity for pathological stroma, sparing healthy tissue.

Conventional antifibrotics act broadly and are dose-limited by systemic toxicity. Viventia's strategy is to engage the activated stromal compartment with precision — targeting pharmacological activity at sites of active fibrogenesis while preserving normal tissue homeostasis and host immunity.

Selectivity

Disease-restricted engagement

Directed at markers enriched on activated, disease-associated fibroblasts and largely absent from quiescent stroma in healthy adult tissue.

Convergence

One program, many organs

Because activated myofibroblasts are a shared endpoint of fibrosis, a single mechanistic approach is extensible across multiple organ systems.

Translation

Biomarker-guided development

Quantitative pharmacodynamic and patient-stratification biomarkers anchor a closed-loop, evidence-led clinical strategy.

Therapeutic focus

Fibrotic disease across organ systems.

A platform addressing fibroinflammatory indications that share a common stromal biology and carry high unmet need.

Cardiac

Heart failure & cardiac fibrosis

Interstitial and perivascular fibrosis driving HFpEF progression — no approved antifibrotic.

Pulmonary

Idiopathic pulmonary fibrosis

Progressive parenchymal scarring; current agents slow but do not reverse decline.

Hepatic

MASH-associated fibrosis

Hepatic stellate-cell activation and bridging fibrosis advancing toward cirrhosis.

Renal

Chronic kidney disease

Tubulointerstitial fibrosis as the common pathway to progressive renal failure.

Dermal & systemic

Systemic sclerosis

Multi-organ fibrosis with limited disease-modifying options.

Pipeline

A focused lead program in active development.

Our first asset advances the platform's precision-targeting strategy toward the clinic. Additional programs remain in earlier discovery.

Program
Discovery
Asset Dev
Lead Opt
IND-enabling
Clinical
VIV-01Lead asset
Fibrotic disease · indication undisclosed

VIV-01 is in active asset development. All programs are pre-clinical.

Our conviction

“Target the cells that drive fibrosis — precisely.”

Get in touch

Partnering & investment.

We welcome conversations with investors and pharma/biotech partners. Detailed materials are available under confidentiality.

team@viventia.bio