Confronting Human Protease-Driven Diseases
Verra transforms the treatment of protease-driven diseases, from COPD to cancer, using an innovative small protein platform.
Verra transforms the treatment of protease-driven diseases, from COPD to cancer, using an innovative small protein platform.
Cancer immunotherapies, often in combination with chemotherapy, have emerged as standards of care for multiple tumor types. Despite breakthrough successes, response rates are still frequently low and cancer recurrences are common.
Cell surface antigen proteins are common targets for intervention. But antigen availability is often dictated by regulatory proteases, and key protease up-regulation is correlated with poor patient outcomes. These facts have been insufficiently appreciated.
Verra’s lead inhibitor, VTH144, is a small protein which will allow immunotherapies to benefit more patients by revitalizing antigen availability.
Tumor proliferative factors are also brought under control with the administration of VTH144 and it promises excellent synergy with chemotherapy (as shown).
Across numerous indications and modalities, Verra intends to leverage and amplify the power of emerging anti-cancer therapies... with real-world impact for poorly responding patients in need.
COPD is a debilitating disease affecting about 384 million people world wide. Spending on drug therapies exceeds 10.6 billion. Health care costs in the US alone exceed $30 billion annually. Sadly, current treatments address primarily symptoms: there are still no disease modifying agents and COPD remains a huge unmet medical need.
What’s new? A specific protease has been definitively linked with COPD’s three most important phenotypes (emphysema, small airway fibrosis and mucous hyper-secretion) and it is up-regulated in the lungs of human COPD patients in proportion to the severity of their disease.
Verra Therapeutics has developed a highly selective and stable inhibitor for this target. Efficacy studies in mice show VTH245’s great potential to block damage in the lung. VTH245 exhibits favorable drug-like pharmacokinetics and is compatible with inhaled routes of administration. Despite an intensely competitive funding environment, Verra enjoys substantial NIH support. Among numerous disease-modifying responses, harmful elastin degradation is blocked in smoke-exposed mice treated with VTH245.
Verra's Inhibitors are based on nature's elegant design for each target and are lightly modified for stability, solubility, potency and good pharmacokinetics.
As native protein drugs, they promise reduced immunogenicity and a smooth regulatory path.
Additional advantages include:
1) Selectivity vastly superior to small molecules... which consistently fail to discriminate between related proteases.
2) Better than antibodies:
- smaller (one ninth the size of antibodies)
- bind only to activated targets
- promise vastly superior tissue and tumor penetration
Incomplete penetration causes reduced efficacy and/or cancer recurrences.
3) Inhaled administration possible (respiratory indications)
4) Simpler microbial production
5) Rapid lead development
6) Broadly applicable, excellent IP protection
Decades of senior leadership managing technology and technology companies.
Biotech and pharmaceutical development experience at the founder, senior executive and board level. Phyton Inc./Phyton Biotech, CellFor Inc., Annikki GmbH and Verra Therapeutics.
Former Oncology Project Lead at GlaxoSmithKline
Comprehensive research background in drug discovery and development.
Renown thought leader on proteases as disease targets.
Extensive industrial experience.
Technology and drug development professional with three decades of experience.
Operational experience across research, drug development and process development.
Associate Professor of Medicine, Harvard Medical School
Broad background in proteases and their roles in regulating lung inflammatory injury.
First to show up-regulation in human COPD lungs and protection in knock-out mice from cigarette smoke-exposure.
Assistant Professor of Radiology, Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School
In vivo context-dependent action of anticancer drugs, proteases, and cell-signaling pathways, with special emphasis on using computational modeling and microscopy methods to understand drug pharmacology
Professor, Molecular & Integrative Physiology, Internal Medicine University of Michigan Medical School
Molecular origins of pancreatic and other cancers.
Crosstalk between cancer and immune cells and the plasticity that leads to resistance and metastasis.
Understanding pathways that promote tumor aggressiveness.
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