One disease hardens the skin; another progressively impairs lung function. These seemingly distant conditions share a process called fibrosis: the excessive accumulation of material that supports tissue.
The 3D-MOFIB research programme, introduced by the NIH's National Center for Advancing Translational Sciences, or NCATS, aims to use this common ground to find drugs. Its initial focus is scleroderma and pulmonary fibrosis associated with Hermansky–Pudlak syndrome. Researchers plan to build three-dimensional skin and lung models from patient-derived fibroblasts, test many compounds in them and examine changes associated with fibrosis.
The plan includes analysing proteins and metabolites as well as gene expression. Finding molecular processes shared across diseases could point towards treatments useful in more than one condition. NCATS description ↗
The question we want to consider is which disease a particular drug should be developed to treat.
If the same candidate works in both skin and lung models, researchers can investigate whether it acts on a shared disease process. If it works in only one, that could provide clues to differences in the local tissue environment or the pathways that lead to fibrosis. Either result could inform where to take the drug next.
Activity in a cultured model does not, of course, establish that a drug can treat several diseases. Even so, there is a reason to study different disease processes side by side from the discovery stage, rather than finding a candidate first and only then asking whether it could be used elsewhere.
What interests us about this programme is not just how sophisticated the engineered tissues become. It is whether comparing skin and lung models produces evidence that could support a drug's use in a broader range of diseases.
Keep following this topic
v1 ·Looking across diseases for drugs that treat fibrosis
3D-MOFIB plans to begin with scleroderma and pulmonary fibrosis associated with Hermansky–Pudlak syndrome, screening compounds and molecular activity in patient-derived models to explore shared fibrosis mechanisms and organ-specific differences.
- Research plan describedRecorded
- Test shared and distinct responsesUnverified
- Inform indication selectionUnverified
Hypothesis and what would change it
Comparing disease contexts during discovery may reveal earlier whether to broaden an indication or pursue organ-specific development paths.
What would change our view: Reconsider use in indication decisions if between-model responses do not reproduce or are explained by culture variability rather than disease or organ differences.
This is a research plan, not demonstrated efficacy or indication expansion. Whether model responses correspond to clinical effects requires separate assessment.
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Evidence & reading
Public sources checked for this edition. Linked pages may subsequently change.
- 3D-MOFIB: human-based models for fibrotic diseases ↗NIH / NCATS · 2026-10-13
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