NVP-13 / TGFBR2
Translating disease mechanisms into targeted interventions.
Explore the biology01 / Our focus
Angalbio develops novel therapeutics by translating disease mechanisms into targeted interventions, with current programs focused on pathological TGF-β signaling in neurodegenerative and fibrotic disease.
The biology behind our approach02 / Flagship program
An LNA-gapmer antisense oligonucleotide designed to reduce TGFBR2 expression.
03 / One program. Two biological branches.
01 / NVP-13 · CNS
In human neural precursor cells, NVP-13 reduced TGFBR2 and pSMAD2, a marker of TGF-β signaling. We are investigating its potential in ALS with Qilu Hospital.
Explore the CNS branch
02 / NVP-13 · Tissue biology
Exploring the relationship between persistent TGF-β signaling, matrix accumulation and maladaptive tissue repair. The therapeutic hypothesis requires validation in each disease setting.
Explore the fibrosis branch
04 / Discovery
Functional biology, molecular therapeutic evaluation and translational research support a broader discovery effort around our lead program.
Explore our discovery approach05 / Pipeline
| Program / target | Disease branch | Public evidence |
|---|---|---|
| NVP-13TGFBR2 · Antisense | Neurodegeneration | Published preclinical research Current development-stage wording awaits company confirmation. |
| NVP-13TGFBR2 · Antisense | Fibrosis | Therapeutic hypothesis Indication-specific development status awaits company confirmation. |
The cited publications do not establish the current IND, clinical-trial or regulatory status.
06 / Selected evidence
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/s13311-021-01045-2Angalbio / Company