A new therapeutic space:
Fibrotic barrier breakers
A novel drug class:
Senolytic ADCs
Two incurable diseases:
Stroma rich cancers and advanced fibrosis
In multiple digestive cancers:
Preclinical proof of concept
Our lead program:
Advancing toward IND in hepatocellular carcinoma
More applications:
Expansion program in liver fibrosis
Our seasoned team:
Built for execution and impact
We design and develop senolytic ADCs, a novel class of antibody-drug conjugates that selectively kill cancer cells and pathogenic senescent cells.
Through this unique two-in-one approach, we aim to tackle highly fibrotic cancers and severe fibrosis.
A new class of ADCs
We have identified a key surface biomarker shared by senescence and cancer cells and engineered high-precision ADCs that kill both cell types to break down the fibrotic barrier that fuels disease progression and treatment resistance.
A new therapeutic space in oncology and fibrosis
Unlock access to inaccessible tumors and enable fibrotic tissue repair.
A timeline convergence
A unique alliance between aging science, translational oncology and ADC engineering to tackle one of clinical's toughest frontiers : cracking therapy-resistant microenvironements in oncology and fibrosis.
About
DPP4: a highly promising biological gateway for precision senolytic therapies
At StarkAge, we start with a simple conviction: to defeat some of the most complex and heterogeneous diseases, you must first identify the master key that drives them with precision. DPP4 (dipeptidyl peptidase-4) offers exactly that: a dual biomarker that sits at the crossroads of cellular senescence, cancer and fibrosis, opening the way to a novel class of ADCs.
A key driver of cancer
Beyond senescence, DPP4 is deeply implicated in cancer biology and drug resistance. Its expression pattern and functional impact make it a strategic vulnerability, especially in hard-to-treat solid tumors:
Overexpressed in both stromal and cancer cells
Marks highly fibrotic tumor microenvironment
Linked to poor outcomes across multiple solid tumors
Fuels tumor growth, survival and proliferation
Enables immune escape, weakening immunotherapy response
Drives migration, invasion and metastasis
Together, these stromal and tumor-intrinsic roles make DPP4 a promising target to tackle hard-to-treat cancers locked in a highly fibrotic microenvironment.
A central role in fibrotic diseases
DPP4 also drives fibrosis by promoting pro-scarring fibroblast activation, pro-fibrotic inflammation and collagen-rich extracellular matrix deposition. Consistent with this central role, its expression correlates with disease severity across major fibrotic conditions, including liver fibrosis, systemic sclerosis and idiopathic pulmonary fibrosis.
StarkAge’s DPP4 ADC is designed to selectively eliminate senescent cells and overactive fibroblasts that keep chronic inflammation alive, aiming to stop disease progression and clear the way for tissue regeneration.
A hallmark of cellular senescence
Senescent cells accumulate with age and stress (notably after exposure to first-line cancer therapy). They secrete a cocktail of inflammatory molecules (cytokines, chemokines, growth factors and proteases) that can help tissue repair but also fuel organ dysfunction, especially inflammatory diseases and cancers.
DPP4 is a defining feature of these cells, functioning as:
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A near-universal surface marker of senescent cells,
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An enzyme that reshapes the local secretory microenvironment,
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An immune-regulatory surface protein.
This profile makes DPP4 a highly actionable target for precision senolysis. Today, StarkAge designs and develops tailored senolytic ADCs to kill pathological cells and stop toxic signaling in fibrotic cancers and advanced fibrosis.
Science
Fibrotic barrier breakers
Senescent cells
SASP = cytokines, chemokines,
growth factors, proteases
Natural aging and/or stress
Oxidative, cancer therapy…
Tissue regeneration
and modeling
Tissue dysfunction
Diabetes, retinopathy...
Inflammatory diseases
Fibrosis, osteoarthritis...
Cancer
Tumor promotion
Immune evasion
Drug AEs & resistance
Senolytic ADCs
Kill pathological cells & stop toxic signaling
Lead program
STX-01
STX-01 is a sole-in-class senolytic ADC combining a high-affinity anti-DPP4 antibody, an exatecan-derived topoisomerase I inhibitor payload and a cathepsin-cleavable linker. Its mechanism of action is unique among all marketed and development-stage ADCs, enabling STX-01 to simultaneously:
Clear senescent cells that fuel inflammation, fibrosis, and therapeutic resistance
Shrink tumors by directly killing malignant cells
Break tumor-stroma crosstalk, a key driver of immune exclusion
Break the fibrotic barrier to reach the tumor
Trigger long-term immune response
Kill cancer cells directly
Community
Leadership:
Florence Lhospice
Executive President
PharmD, PhD
Co-founder and CDO at Emergence Therapeutics (acquired by Eli Lilly in 2024), specialist in ADC development (CMC and regulatory).
Benjamin Le Calvé
Chief Executive Officer
PhD
Postdoctoral experiences in senescence (Lyon and Montreal). Expert in the development of targeted therapies.
Scientific Advisory Board
Cleo Bishop
BSc, PhD
Professor of Senescence at Queen Mary University of London. Director of QMUL at Blizard Institute.
François Romagné
PhD
Founder of Innate Pharma and Mimabs. Professor of immunotechnology at Aix-Marseille University. Specialist in antibody and ADC development.
Fabrizio d’Adda di Fagagna
PhD
Head of cellular senescence team at FIRC Institute of Molecular Oncology.
Partners
Since its inception, StarkAge has been open to partnerships with leading institutions able to facilitate and accelerate the development of its new drug class. Accordingly, the company benefits from a scientific and clinical partnership with Gustave Roussy, one of Europe’s leading cancer centers. This collaboration strengthens StarkAge’s translational strategy by providing access to world-class expertise in tumor biology, senescence and immuno-oncology, as well as clinical insight to guide indication selection and trial design.