SCD1 x PPARα

Last update 08 May 2025

Basic Info

Related Targets

SCD1PPARα

Drugs associated with SCD1 x PPARα

TD07-AFC2

Target

PPARα x SCD1

Mechanism

PPARα modulators [+1]

Active Org.

Tissue Dynamics Ltd.

Originator Org.

Tissue Dynamics Ltd.

Active Indication

Myocardial fibrosis

Inactive Indication-

Drug Highest PhasePhase 1

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with SCD1 x PPARα

100 Translational Medicine associated with SCD1 x PPARα

0 Patents (Medical) associated with SCD1 x PPARα

286

Literatures (Medical) associated with SCD1 x PPARα

01 Jul 2025·Prostaglandins, Leukotrienes and Essential Fatty Acids

Fatty acid synthase global inducible knockout does not alter brain fatty acid concentrations but attenuates cholesterol synthesis in the adult mouse

Article

Author: Seeger, Drew R ; Golovko, Mikhail Y ; Golovko, Svetlana A ; Kotha, Peddanna ; Murphy, Eric J

Fatty acid (FA) de novo synthesis, also called de novo lipogenesis (DNL), has a central role in peripheral energy storage and provides structural components for lipid membranes. However, less is known regarding its contribution to brain FA homeostasis. DNL is catalyzed by fatty acid synthase (FAS), which is a multifunctional enzyme expressed in all mammalian tissues. In the present study, we addressed, for the first time, the effect of FAS gene global conditional inducible knockout (Fasn KO) on the adult brain FA concentrations and lipid metabolism. We achieved a 67 % reduction in the brain FAS protein levels, with a significant reduction in total FA synthesis measured by ³H₂O incorporation into FA, which was lethal 10 days after gene recombination induction. However, the concentrations of all 44 FA molecular species assayed by LC-MS were unchanged in the brain. We also did not detect changes in the major proteins involved in FA synthesis regulation and remodeling, including peroxisome proliferator-activated receptor α (PPARα), PPARδ, FA desaturase-1, -2, and -3, and Stearoyl-CoA desaturase 1 but did observe a decrease in PPARɣ levels. In addition, brain cholesterol synthesis was significantly reduced in the Fasn KO brains. These data indicate that DNL is not required to maintain measured FA concentrations in the brain and that dietary FA and liver-derived pools might compensate for decreased brain DNL within the duration of the study. However, our data indicate a possible role of FAS in PPARɣ regulation and cholesterol metabolism in the adult brain.

01 Jun 2025·Regulatory Toxicology and Pharmacology

Next generation risk assessment of hair dye HC yellow no. 13: Ensuring protection from liver steatogenic effects

Article

Author: Rogiers, Vera ; Heymans, Anja ; Sepehri, Sara ; Van Goethem, Freddy ; De Win, Dinja ; Vanhaecke, Tamara ; Rodrigues, Robim M

This study employs animal-free Next Generation Risk Assessment (NGRA) principles to evaluate the safety of repeated dermal exposure to 2.5% (w/w) HC Yellow No. 13 (HCY13) hair dye. As multiple in silico tools consistently flagged hepatotoxic potential, likely due to HCY13's trifluoromethyl group, which is known to interfere with hepatic lipid metabolism, liver steatosis was chosen as the primary mode of action for evaluation. AOP-guided in vitro tests were conducted, exposing human stem cell-derived hepatic cells to varying HCY13 concentrations over 72 h. The expression of 11 lipid metabolism-related marker genes (AHR, PPARA, LXRA, APOB, ACOX1, CPT1A, FASN, SCD1, DGAT2, CD36, and PPARG) and triglyceride accumulation, a phenotypic hallmark of steatosis, were measured. PROAST software was used to calculate in vitro Points of Departure (PoD_NAM) for each biomarker. Using GastroPlus 9.9, physiologically-based pharmacokinetic (PBPK) models estimated internal liver concentrations (C_{max liver}) of HCY13, ranging from 4 to 20 pM. All PoD_NAM values significantly exceeded the predicted C_{max liver}, indicating that HCY13 at 2.5% (w/w) is unlikely to induce liver steatosis under the assumed conditions. This research demonstrates the utility of NGRA, integrating AOP-based in vitro assays and computational models to protect human health and support regulatory decision-making without animal testing.

01 May 2025·International Journal of Biological Macromolecules

Buckwheat resistant starch alleviates hyperlipidaemia in mice by inhibiting lipid accumulation and regulating gut microbiota

Article

Author: Bu, Tongliang ; Li, Qingfeng ; Tao, Jiwen ; Yuan, Ming ; Zhang, Xinyu ; Chen, Zhao ; Li, Zhenjiang ; Tang, Zizhong ; Jia, Yujie ; Xiao, Yirong ; Bai, Hongjie ; Xie, Qiqi

Hyperlipidemia, a prevalent metabolic disorder disease, has become a significant global health challenge. In this research, we looked into the effects of buckwheat resistant starch (BRS) supplementation on lipid metabolism and gut microbiota in hyperlipidemic mice. Results showed that HBRS intervention significantly inhibited weight gain in high-fat diet mice, reducing body weight by 2.91 g versus MC group. Serum TC, TG, and LDL-C decreased by 74.25 %, 76.79 %, and 56.25 % respectively, while HDL-C increased by 67.66 %. HBRS mitigated hepatic steatosis and epididymal adipocyte hypertrophy. HBRS downregulated TNF-α and IL-6 by 24.4 % and 18.25 %, respectively, and upregulated IL-10 by 15.35 %. It modulated lipid metabolism genes by suppressing SREBP2, FAS, SCD1 and activating PPARα/CPT1. Moreover, BRS improved gut microbiota composition by lowering the F/B ratio and enhancing populations of SCFA-producing bacteria (e.g., Akkermansia, Bifidobacterium, and Parabacteroides). BRS significantly increased the total levels of SCFAs in the gut. Compared to the MC group, HBRS resulted in increases of 40.2 %, 51.8 %, and 68.3 % in acetate, propionate, and butyrate, respectively. Collectively, these results demonstrate that BRS serves as a beneficial nutritional resource for the management of hyperlipidemia.

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