Publications
Research papers on NVP-13 and independent studies of TGF-β biology, with study type and limitations noted.
Showing 12 publications
NVP-13 · Preclinical research
In healthy non-human primates, intrathecal NVP-13 reduced CNS TGFBR2 expression and changed neurogenic-niche measures. This was not an ALS disease model or a test of patient benefit.
DOI: 10.1007/s13311-021-01045-2NVP-13 · Preclinical research
Reports reduced TGFBR2 RNA and protein and lower pSMAD2 in human neural precursor and lung-derived cell models. These cell findings do not establish clinical safety or efficacy.
DOI: 10.3390/ijms21061952NVP-13 · Non-GLP monkey study
Reports a phased non-GLP intrathecal NVP-13 toxicity and pharmacokinetic program in healthy cynomolgus monkeys. It does not test ALS efficacy or establish human safety.
DOI: 10.3390/app12030973NVP-13 · GLP monkey study
Reports a 13-week GLP repeated-dose intrathecal toxicity study in healthy cynomolgus monkeys. The paper title is retained verbatim; its findings do not establish clinical safety or therapeutic benefit.
DOI: 10.3390/pharmaceutics14010200Independent literature · ALS mouse study
In SOD1G93A ALS mice, a TGF-β signaling inhibitor given after disease onset extended survival. The intervention was not NVP-13 or a TGFBR2-targeting ASO.
DOI: 10.1016/j.celrep.2015.03.053Independent literature · ALS mouse study
In an ALS mouse model, early treatment with the TGF-β pathway inhibitor halofuginone delayed deterioration and prolonged survival. Halofuginone is not NVP-13 or a TGFBR2-selective ASO.
DOI: 10.1111/jnc.16102Independent literature · Unreviewed CSF preprint
CSF proteomics found stage-associated TGFBR2 changes and associations with poorer function and longer disease duration. This preprint does not, from the reported text alone, establish a general ALS-versus-control increase.
DOI: 10.64898/2026.04.13.26350753Independent 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.70227Angalbio & JLP Health · Target discovery
Angalbio and JLP Health authors used forward genetics to identify ATP1A1 as a periplogenin target in prostate-cancer models. This is a discovery-platform study, separate from NVP-13.
DOI: 10.1038/s41598-024-71722-7Independent 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.2016.48Publication titles retain their original wording. Independent studies provide biological context and are not presented as Angalbio-sponsored NVP-13 research.