Modified auristatin compounds restore potency while preserving anti-mitotic activity to inhibit tumor growth and kill cancer cells.
Stabilizing Atoh1 by inhibiting proteasome degradation and related epigenetic pathways helps regenerate sensorineural hair cells for hearing loss.
Low-dose ATRA, ATO, and Bortezomib combine ER stress, oxidative stress, and proteasome inhibition to kill FLT3-ITD+ AML cells with lower toxicity.
A four-drug animal formulation improves cardiac output, lowers pulmonary pressure, and helps prevent right heart failure.
Intra-hepatic delivery of engineered NK cells improves liver tumor targeting, boosts cytotoxicity, and limits off-target toxicity.
Short sardine peptides inhibit mast cell degranulation and inflammation to relieve allergic rhinitis without irritation, dryness, or drowsiness.
Genetic screening for ATAD1 loss identifies cancers more susceptible to proteasome inhibitors, improving apoptosis targeting and treatment use.
A WA-C-WB bifunctional ligand recruits two proteins into one complex, boosting binding potency for targets that lack deep binding pockets.
Novel thiazole acrylate PRX3 inhibitors address thiostrepton insolubility and synthesis complexity while retaining cancer cell killing activity.
Blocking Notch signaling with gamma-secretase inhibitors reduces collagen deposition and fibrotic markers in RDEB fibroblasts.
A zinc salt and cyclo-hispro blend reduces allergic cytokines and mucus secretion to treat respiratory disease with fewer side effects.
A bifunctional PROTAD compound degrades EGFR via ubiquitination to overcome mutation-driven resistance and suppress tumor progression.
A nine-ingredient unit dose targets gut inflammation, microbiota imbalance, and intestinal barrier weakness to improve gastrointestinal health.
Engineered NK cells with cytotoxic receptors and local liver delivery improve tumor infiltration and killing in liver tumors.
Activating growth factor receptors with a bioactive carrier converts neoplastic cells toward functional states while limiting healthy-cell damage.
Selective IBAT inhibition blocks ileal bile acid re-absorption, lowering bile acid burden and improving liver histology and function.