Fibrosis
Exploring persistent signaling, extracellular-matrix accumulation and maladaptive tissue repair.
Persistent TGF-β signaling, matrix accumulation and maladaptive repair provide a biological rationale for investigating TGFBR2 modulation. Physiological tissue repair remains essential; the question is where intervention may be useful.
Two liver-fibrosis mouse studies report that deleting Tgfbr2 specifically in hepatocytes or endothelial cells reduced fibrotic changes. These genetic results are cell- and model-specific, not evidence of NVP-13 efficacy.
Exposure, target modulation and functional benefit are different questions. Each requires disease-specific evidence.
Explore the NVP-13 approachNVP-13 / TGFBR2
The fibrosis branch is a therapeutic hypothesis. Indication-specific development status and the public scope of specific fibrosis indications remain to be confirmed.
Public evidence and development statusIndependent literature · Liver mouse study
Hepatocyte-specific Tgfbr2 deletion reduced profibrotic markers and improved hepatic function in a CCl4 mouse model. Genetic deletion is not NVP-13 treatment.
DOI: 10.1111/1751-2980.13161Independent literature · Liver mouse study
Endothelial-specific Tgfbr2 deletion attenuated fibrosis and inflammation in experimental liver-injury mouse models. This does not establish the effect of systemic or tissue-directed NVP-13.
DOI: 10.1111/liv.70227Independent literature · Mouse study
In a mouse lung-injury model, fibroblast-specific Tgfbr2 deletion reduced fibrosis but increased early inflammation and mortality. This does not test NVP-13.
DOI: 10.1038/s41586-024-07660-1Independent literature · Review
A review of TGF-β signaling in kidney fibrosis, not primary evidence for NVP-13 or any proposed fibrosis indication.
DOI: 10.1038/nrneph.2016.48