Journal: Molecular cell

Article Title: Lipidomic Analysis of α-Synuclein Neurotoxicity Identifies Stearoyl CoA Desaturase as a Target for Parkinson Treatment

doi: 10.1016/j.molcel.2018.11.028

Figure Lengend Snippet: A) Lipid profiles of vector and human αS expression in yeast 12 h post induction. Lipid species (116) indicated by color and in the order of the key. B) Primary pathway for LD formation. DG and TG metabolic pathways are highly conserved between mammals (enzymes-red) and yeast (enzymes-blue). ACC1, cytosolic acetyl-CoA carboxylase; ATGL, adipose triglyceride lipase; DGAT1, 2: diacylglycerol acyltransferases; DGK, diglyceride kinase (multiple isoforms in mammals); OA, oleic acid; HSL, hormone-sensitive lipase; LCAT, lecithin:cholesterol acyltransferase; Seipin, integral membrane protein; SCD1, stearoyl-coA-desaturase; LPIN, lipid phosphatases; ER, endoplasmic reticulum; LD, lipid droplet. Whether lipolysis-derived DG enters the ER is currently unknown. C) αS expression increases LD formation in yeast. Green: BODIPY (LDs). Bar chart: integrated density (ImageJ) fold difference of uninduced vs induced (12h post induction). n = 22/condition. p<0.0005, t-test. D) LDs (TG) protect against αS toxicity. Differences in αS toxicity in 4 different strain backgrounds: (i) wt; (ii) dga1Δ lro1Δ; (iii) are1Δ are2Δ; (iv) LDΔ = dga1Δ lro1Δ are1Δ are2Δ. Samples induced at 5 nM estradiol. Table S2: statistical analysis of all yeast growth curves.

Article Snippet: M17D-TR/αS-3K::YFP//RFP cells were treated with Scd1 inhibitor 24 h after plating on 384-well plates, at 1 or 10μM (HY19762 or HY15700, MedChemexpress) and immediately induced via dox, followed by Incucyte-based analysis.

Techniques: Plasmid Preparation, Expressing, Derivative Assay

Journal: Molecular cell

Article Title: Lipidomic Analysis of α-Synuclein Neurotoxicity Identifies Stearoyl CoA Desaturase as a Target for Parkinson Treatment

doi: 10.1016/j.molcel.2018.11.028

Figure Lengend Snippet: A) Lipid profiles of human αS expression in rat cortical neurons. Lipid species (516) are indicated by color and in the order of the key on the right of the map. B) αS expression increases LD formation in rat cortical neurons. Microscopy-Green: BODIPY (LDs); Red: αS. Blue: Hoechst (nucleus). Neurons were imaged at 14d (ImageJ quantified). Bar chart: integrated density signal fold difference for MOI1 vs MOI5. n=16 cells. p<0.0001,t-test. C) LDs protect against αS toxicity in rat cortical neurons. Neuronal survival was measured following expression of αS in control rat cortical neurons and in neurons with knockdown of DGAT1 and DGAT2 (D1+D2). Fig S3E, RTPCR knockdown data. % Viability (Resazurin to Resorufin conversion). n=6. ****p<0.0001 *p=0.02 (one way Anova). D) Reduction in LPIN expression suppresses αS toxicity in rat cortical neurons. Neuronal survival was measured following expression of αS in control rat cortical neurons and in neurons with knockdown of LPIN1, LPIN2, LPIN3. Fig S3F, RTPCR knockdown data. %Viability (Resazurin to Resorufin conversion). n=6 ****p<0.0001 **p=0.007 (one way Anova). E) OA content is increased upon human αs expression in rat cortical neurons. Intracellular FA analysis was performed in control and human αS expressing rat cortical neurons. *p=0.02, t-test. F) Reduction in SCD1 rescues αS toxicity. Neuronal survival was measured following expression of human αS in control rat cortical neurons and in neurons with SCD1 knockdown. Fig S4E, RT-PCR knockdown data. % Viability (Resazurin to Resorufin conversion). n=6. ****p<0.0001 (one way Anova). G) Inhibition of SCD1 rescues αS toxicity (% ATP). Survival of neurons was measured following treatment with SCD1 inhibitor in control and human αS-expressing rat cortical neurons. ****p<0.0001 ***p≤0.0005 (one way Anova). H) SCD1 inhibition rescues DGAT1+DGAT2+αS-associated toxicity in rat cortical neurons. DGAT1 and DGAT2 (D1+D2) were knocked down in control vs human αS-expressing rat cortical neurons + DMSO or SCD inhibitor. %Viability (Resazurin to Resorufin conversion). n=6. ***p<0.0005 (one way Anova). I) SCD knockdown in a C. elegans model of dopaminergic neuron degeneration rescued an αS-induced dopaminergic neuron degeneration phenotype. Open arrowheads-CEP dendrites (white), ADE dendrites (black);closed arrowheads-CEP cell bodies (white), ADE cell bodies (black); *p<0.05.

Article Snippet: M17D-TR/αS-3K::YFP//RFP cells were treated with Scd1 inhibitor 24 h after plating on 384-well plates, at 1 or 10μM (HY19762 or HY15700, MedChemexpress) and immediately induced via dox, followed by Incucyte-based analysis.

Techniques: Expressing, Microscopy, Reverse Transcription Polymerase Chain Reaction, Inhibition

Journal: Molecular cell

Article Title: Lipidomic Analysis of α-Synuclein Neurotoxicity Identifies Stearoyl CoA Desaturase as a Target for Parkinson Treatment

doi: 10.1016/j.molcel.2018.11.028

Figure Lengend Snippet: A) Exogenous OA increases αS inclusions in αS3K-expressing neuroblastoma cells. *p<0.05 ****p<0.0001 (one way Anova). B) SCD1 knockdown decreases αS inclusions in αS3K-expressing neuroblastoma cells. C: control (scrambled DsiRNA). ***p<0.0005; ****p<0.0001. C) SCD inhibition decreases αS inclusions. *p<0.05 ****p<0.0001 (one way Anova). D) SCD inhibition decreases αS inclusions (microscopy) in αS3K-expressing neuroblastoma cells. E&F) SCD1 inhibition increases 60kDa αS:14kDa αS in αS3K-expressing neuroblastoma cells. *non-specific band (Perrin et al., 2003).*p<0.05 **p<0.01. G) SCD inhibition decreases pS129 αS: total αS. n=6. *p<0.05 ***p<0.005,t-test. H) SCD1 inhibition increases 60kDa αS:14kDa αS and 80kDa αS: 14kDa αS in fPD E46K-expressing neuroblastoma cells. N=2, n=6. I) SCD1 inhibition decreases pS129 αS: total αS in E46K-expressing cells. N=2, n=10. **p<0.01, t-test.

Article Snippet: M17D-TR/αS-3K::YFP//RFP cells were treated with Scd1 inhibitor 24 h after plating on 384-well plates, at 1 or 10μM (HY19762 or HY15700, MedChemexpress) and immediately induced via dox, followed by Incucyte-based analysis.

Techniques: Expressing, Inhibition, Microscopy

Journal: Molecular cell

Article Title: Lipidomic Analysis of α-Synuclein Neurotoxicity Identifies Stearoyl CoA Desaturase as a Target for Parkinson Treatment

doi: 10.1016/j.molcel.2018.11.028

Figure Lengend Snippet:

Article Snippet: M17D-TR/αS-3K::YFP//RFP cells were treated with Scd1 inhibitor 24 h after plating on 384-well plates, at 1 or 10μM (HY19762 or HY15700, MedChemexpress) and immediately induced via dox, followed by Incucyte-based analysis.

Techniques:

Journal: medRxiv

Article Title: Amelioration of non-alcoholic fatty liver disease by targeting G protein-coupled receptor 110: A preclinical study

doi: 10.1101/2022.12.07.22283206

Figure Lengend Snippet: Primary hepatocytes were isolated from eight-week-old male C57BL/6J mice with STC. (A) Primary hepatocytes were infected with either adenoviral vector expressing GPR110 (ADV-GPR110) or control adenovirus expressing GFP (ADV- GFP) 24h after plating, followed by transfection with ASO1-GPR110, ASO2-GPR110 or ASO-NC for another 6 hours. mRNA expression levels of GPR110 and SCD1 from different groups were assessed, as determined by qPCR analysis. (B) Left panel: immunoblotting analysis for the expression level of GPR110 and SCD1 from different groups of primary hepatocytes. Right panel: quantification of protein expression levels of GPR110 and SCD1. Protein expression levels were normalized to the expression of β-tubulin. Each lane is a sample from a different plate. Right panel: quantification of protein expression levels of GPR110, SCD1 and β-tubulin. n = 3 per group. Protein expression levels were normalized to the expression of β-tubulin. The samples for GFP were set as 1 for fold-change calculation. (C-D) HEK293 cells were infected with pGL3-SCD1 promoter-luciferase plasmid and adenoviral vector expressing GPR110 (ADV- GPR110) or GFP (ADV-GFP) for 48 h and DHEA was added to the transfected cells at the concentration of 100 μM for 24 h. Cell lysates were used for (C) luciferase assay or (D) qPCR analysis. Lysates from the cell co-transfection with pGL3-SCD1 promoter-luciferase plasmid and ADV-GFP without treatment of DHEA was set as 1 for fold-change calculation. (E-G) Primary hepatocytes were infected with either adenoviral vector expressing GPR110 (ADV-GPR110) or control ADV-GFP, followed by transfecting with scramble or shSCD1-1 or shSCD1-2 plasmids for another 72 h. Intracellular lipids were extracted and (E) CHO, (F) TG, and (G) FFA were assessed. STC, standard chow diet; i.v., intravenous injection; s.c., subcutaneous injection; ASO, antisense oligonucleotides. CHO, cholesterol; TG, triglyceride; FFA, free fatty acid. Data represents as mean ± SEM; n = 3 per group; repeated with three independent experiments; P value analysed by two-tailed Student’s t test. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: For SCD1 inhibitor delivery, MK-8245 (MedChemExpress, NJ, USA) was gavaged at 10 mg/kg BW once a week [ ].

Techniques: Isolation, Infection, Plasmid Preparation, Expressing, Control, Transfection, Western Blot, Luciferase, Concentration Assay, Cotransfection, Injection, Two Tailed Test

Journal: medRxiv

Article Title: Amelioration of non-alcoholic fatty liver disease by targeting G protein-coupled receptor 110: A preclinical study

doi: 10.1101/2022.12.07.22283206

Figure Lengend Snippet: Eight-week-old male C57BL/6J mice were infected with either 3×10 11 copies of rAAV encoding GPR110 (rAAV-GPR110, i.v.) or control (rAAV-GFP, i.v.) and SCD1 inhibitor (MK8245, 10 mg/kg BW/week, p.o.) or inhibitor vehicle (inhibitor-Veh., p.o.) received HFD feeding. (A) Schematic illustration of viral treatments. (B) Hepatic mRNA expression levels of GPR110 from different groups of mice received rAAV and inhibitor fed with HFD respectively, as determined by qPCR analysis. (C) Left panel: immunoblotting analysis for the hepatic protein expression level of GPR110 and SCD1 from different groups of mice fed with HFD. Right panel: quantification of protein expression levels of GPR110 and SCD1. Protein expression levels were normalized to the expression of β-tubulin. Each lane is a sample from a different individual; n = 3 per group. (D) Body weight and (E) fasting blood glucose level were measured at different weeks upon rAAV and inhibitor injection. (F) The fasting blood insulin level and (G) HOMA-IR index were measured and calculated according to the formula [Fasting blood glucose (mmol/l) × Fasting blood insulin (mIU/l)]/22.5 for the HFD-fed rAAV-GPR110 or rAAV-GFP mice at the end of the experiment. (H) GTT (1 g/kg BW, left) and AUC (right) of serum glucose at the week of 10. (I) PTT (1 g/kg BW, left) and AUC (right) of serum glucose at week 11. (J) ITT (0.5 U/kg BW, left) and AUC (right) of serum glucose at week of 12. mRNA expression levels of the target genes were normalized to the expression of mouse GAPDH. rAAV- NC group was set as 1 for fold-change calculation. HFD, high-fat diet; i.v., intravenous injection; p.o., oral administration; ASO, antisense oligonucleotides; BW, body weight; GTT, glucose tolerance test; PTT, pyruvate tolerance test; ITT, insulin tolerance test; AUC, area under curve; NC, negative control; HOMA- IR, homeostasis model assessment-estimated insulin resistance. Data represents as mean ± SEM; n = 8 mice per group; repeated with three independent experiments; P value analysed by two-tailed Student’s t test. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: For SCD1 inhibitor delivery, MK-8245 (MedChemExpress, NJ, USA) was gavaged at 10 mg/kg BW once a week [ ].

Techniques: Infection, Control, Expressing, Western Blot, Injection, Negative Control, Two Tailed Test

Journal: medRxiv

Article Title: Amelioration of non-alcoholic fatty liver disease by targeting G protein-coupled receptor 110: A preclinical study

doi: 10.1101/2022.12.07.22283206

Figure Lengend Snippet: Eight-week-old male C57BL/6N mice were infected with either 3×10 11 copies of rAAV encoding GPR110 (rAAV-GPR110, i.v.) or control (rAAV-GFP, i.v.) and administered with SCD1 inhibitor (MK8245, 10 mg/kg BW, p.o.) or inhibitor vehicle (inhibitor-Veh., p.o.) received HFD feeding. (A) Serum CHO, (B) serum TG and (C) serum FFA levels were measured at the end of experiment. (D) Serum HDL and LDL, (E) AST and ALT level of each group of mice were measured at the end of the experiment. (F) The ratio of the liver weight against body weight was calculated after sacrificing the mice from four different groups. (G) Representative gross pictures of liver tissues (upper panels), representative images of H&E (middle panels) and Oil Red O (lower panels) staining of liver sections (200 µm). The percentage of lipid area according to H&E staining (right panel); n = 3 per group. (H) Hepatic CHO, (I) hepatic TG and (J) hepatic FFA were normalized by the weight of liver samples used for lipid extraction. STC, standard chow diet; HFD, high-fat diet; i.v., intravenous injection; p.o., oral administration; CHO, cholesterol; TG, triglyceride; FFA, free fatty acid; HDL, high-density lipoprotein; LDL, low-density lipoprotein; AST, aspartate transaminase; ALT, alanine transaminase; H&E, hematoxylin-eosin. Data represents as mean ± SEM; n = 8 mice per group; repeated with three independent experiments; P value analyzed by two-tailed Student’s t test. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: For SCD1 inhibitor delivery, MK-8245 (MedChemExpress, NJ, USA) was gavaged at 10 mg/kg BW once a week [ ].

Techniques: Infection, Control, Staining, Extraction, Injection, Two Tailed Test

Journal: medRxiv

Article Title: Amelioration of non-alcoholic fatty liver disease by targeting G protein-coupled receptor 110: A preclinical study

doi: 10.1101/2022.12.07.22283206

Figure Lengend Snippet: Hepatic expression of GPR110 is upregulated in obese patients with hepatic steatosis when compared to those with normal liver morphology, which is positively associated with hepatic SCD1 expression level. NAFLD patients have higher hepatic expression of GPR110 accompanied with increased mRNA SCD1 expression. (A) Normalized Log2 mRNA expression of GPR110 in lean people without NAFLD (n = 12), obese people without NAFLD (n = 17) or obese patients with NAFLD (n = 8) according to the GEO database (GEO; Profile # GDS4881 / 8126820). (B) Correlation between GPR110 and SCD1 in liver of human subjects based on the GEO database. (C) Representative images of liver tissues with H&E staining (upper panels) and immunohistochemical staining (IHC) of GPR110 (lower panels) from patients with different degree of NAFLD (200 µm). The percentage of GPR110 positive area according to H&E staining (right panel). The percentage of GPR110 positive areas according to IHC staining (right panel); n = 3 per group. Data represents as mean ± SEM. P value analyzed by two-tailed Student’s t test. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: For SCD1 inhibitor delivery, MK-8245 (MedChemExpress, NJ, USA) was gavaged at 10 mg/kg BW once a week [ ].

Techniques: Expressing, Staining, Immunohistochemical staining, Immunohistochemistry, Two Tailed Test

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: (A) Structure of Aramchol (B) SCD1 converts saturated fatty acids (SFAs) to monounsaturated fatty acids (MUFAs), inhibiting SCD1 results in decreased incorporation of lipid droplets, reduced lipid storage and increased fatty acid oxidation.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: General structural representation of SCD1 inhibitors.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Monocyclic SCD1 inhibitors: piperazinyl – pyridazine based SCD1 inhibitors as reported by Xenon.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Monocyclic SCD1 inhibitors: six-membered piperazinyl based SCD1 inhibitors.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Monocyclic SCD1 inhibitors: pyridazine based carboxamide and acetylene linker containing SCD1 inhibitors.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Monocyclic SCD1 inhibitors: piperidine based SSI-4 and pyridine based SCD1 inhibitors.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Monocyclic SCD1 inhibitors: pyridazine–piperidine containing SCD1 inhibitors reported by Takeda Pharmaceuticals and Yang et al.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Monocyclic SCD1 inhibitors: SCD1 inhibitors reported by Xenon and Merck.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Monocyclic SCD1 inhibitors: SCD1 inhibitors containing 5-membered rings as central moiety.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Monocyclic SCD1 inhibitors: thiazole derivatives as SCD1 inhibitors.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Monocyclic SCD1 inhibitors: five membered heterocycles reported for SCD1 inhibition.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques: Inhibition

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Bicyclic SCD1 inhibitors: development of SAR 707 and SAR 224.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Bicyclic SCD1 inhibitors: various bicyclic heterocycles as potential SCD1 inhibitors.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Spirocyclic SCD1 inhibitors: spiro benzo-oxapine based SCD1 inhibitors.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Spirocyclic SCD1 inhibitors: oxazepane-piperidine based spirocyclic systemic SCD1 inhibitors.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Development of MK-8245 based SCD1 inhibitors.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Tetrazole and thiazole acetic acid based SCD1 inhibitors.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Acyclic linker based liver targeted SCD1 inhibitors.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Spirocyclic liver targeted SCD1 inhibitors.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Natural products based SCD1 inhibitors.

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques:

Journal: RSC Advances

Article Title: An insight into advances and challenges in the development of potential stearoyl Co-A desaturase 1 inhibitors

doi: 10.1039/d4ra06237j

Figure Lengend Snippet: Key developments in SCD1 inhibitors during the last 10 years (2013–2023)

Article Snippet: To develop potential SCD1 inhibitors to treat metabolic diseases, researchers from Novartis and Xenon collaborated in the year 2004.

Techniques: Activity Assay, Inhibition, Binding Assay, In Silico