ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
ND-630, an acetyl-CoA carboxylase inhibitor, prevents renal fibrosis in adenine-induced CKD mice.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- An updated overview of alkaloids for the prevention and treatment of metabolic dysfunction-associated steatotic liver disease.Frontiers in pharmacology · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
To evaluate the protective potential of ND-630, an acetyl-CoA carboxylase (ACC) inhibitor, in preventing renal fibrosis using an adenine-induced chronic kidney disease (CKD) mouse model. Male C57BL/6 mice were divided into four groups: control, CKD, CKD + ND-630 low-dose (4 mg/kg/d), and CKD + ND-630 high-dose (16 mg/kg/d). CKD was induced by feeding 0.2% adenine diet for 4 weeks with concurrent ND-630 treatment. Renal function was assessed by serum creatinine (Scr) and blood urea nitrogen (BUN). Histopathological analysis included PAS and Sirius red staining. Fibrosis markers (α-smooth muscle actin and vimentin), ACC1 expression, lipid deposition, oxidative stress markers (catalase, superoxide dismutase 2, and NADPH oxidase 4), inflammatory cytokines (tumor necrosis factor-α and interleukin-6), and transforming growth factor-β1 (TGF-β1)/Smad signaling were evaluated using immunohistochemistry, ELISA, and immunofluorescence. ND-630 significantly decreased Scr and BUN levels in CKD mice, with greater efficacy at higher doses. Administration of ND-630 limited renal tubular injury and collagen deposition. ND-630 suppressed the expression of fibrosis markers such as α-smooth muscle actin and vimentin, inhibited ACC1 expression, malonyl-CoA production, and lipid accumulation. Additionally, ND-630 protected against oxidative stress, decreased inflammatory cytokines levels, and antagonized TGF-β1/Smad signaling activation in CKD kidneys. ND-630 demonstrates nephroprotective effects in adenine-induced CKD mice by inhibiting ACC1-mediated lipid accumulation, suppressing oxidative stress and inflammation, and antagonizing TGF-β1/Smad signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.