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lipofermata (MedChemExpress)

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MedChemExpress lipofermata
Lipofermata, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/lipofermata/Lipofermata/pm42120478-59-21-22
Average 94 stars, based on 14 article reviews

lipofermata - by Bioz Stars, 2026-10

94/100 stars

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Article Title: Cannabidiol triggers fatty acids β-oxidation mediated by Stat2 to facilitate intestinal stem cells regeneration post radiation.
Article Snippet: Before IR (8 Gy, 0.6 Gy/min), organoids were treated with CBD (10 μM), GW6471 (MedChemExpress, 4 μM), GW590735 (MedChemExpress, 1 nM), lipofermata (MedChemExpress, 10 μM), 10,12- tricosadiynoic acid (MedChemExpress, 1 μM), γ-linolenic acid (MedChemExpress, 2 μM), α-linolenic acid (MedChemExpress, 2 μM), eicosapentaenoic acid (EPA) (MedChemExpress, 2 μM) and cis-9-palmitoleic acid (SigmaAldrich, 3 μM).

Derivative Assay:

Article Title: Fatty acid transport protein-2 inhibition enhances glucose tolerance through α-cell-mediated GLP-1 secretion
Article Snippet: Experiments were conducted according to previously described 353 methods (20), using a QBT assay (Molecular Devices). .. Briefly, αTC1-6 cells (ATCC), which were 354 originally derived from mouse pancreatic α-cells (64), were seeded in 96-well plates, and 355 cultured to confluence over 24 h. Wells were washed with serum-free, phenol-free media for 2 356 h at 37o C; Lipofermata (5-bromo-5ʹ-phenylspiro[ 357 3H-1,3,4-thiadiazole-2,3ʹ-indoline]-2-one) (MedChemExpress) was robotically incubated for the 358 final hour. .. BODIPY-conjugated C18 fatty acids (Molecular Devices QBT assay, 2.5 μM complexed 359 with 0.2 % fatty acid-free albumin carrier + FATP2 inhibitors in QBT loading buffer that contains a 360 proprietary external quenching dye) were robotically added at time = 0.

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Article Title: Fatty acid transport protein-2 inhibition enhances glucose tolerance through α-cell-mediated GLP-1 secretion
Article Snippet: .. Initial incubations included modified Krebs buffer supplemented with 385 2.8 mM glucose (37o C, 1 hr) plus linagliptin (MedChemExpress; 100 nM) ± palmitate (Avanti; 386 100-400 μM complexed with 0.2% delipidated albumin), Lipofermata (MedChemExpress; 50387 μM), or exendin[9-39] (MedChemExpress; 100 nM). ..

Article Title: Fatty acid transport protein 2 inhibition enhances glucose tolerance through α cell–mediated GLP-1 secretion
Article Snippet: .. Initial incubations included modified Krebs buffer supplemented with 2.8 mM glucose (37°C, 1 hour) plus linagliptin (MedChemExpress; 100 nM) with or without palmitate (Avanti; 100–400 μM complexed with 0.2% delipidated albumin), lipofermata (MedChemExpress; 50 μM), or exendin[9-39] (MedChemExpress; 100 nM). ..

Staining:

Article Title: Acidosis Forces Fatty Acid Uptake and Metabolism in Cancer Cells Regardless of Genotype
Article Snippet: [ ] Similarly, LD quantification was performed in bovine aortic endothelial cells and cardiomyocytes cultured in either 21% or 1% O 2 conditions (H35 Hypoxystation, Don Whitley Scientific). .. For live cell BODIPY staining, 20 000 7.4 > cancer cells were seeded in μ‐slide 8 well high (80 806, Ibidi) and treated the day after with 7.4 or 6.5 pH medium containing 50 μ m DHA in combination or not with 2 μg mL −1 JC63.1 (ab23680; Abcam), 10 μ m SSO (SML2148, Merck), 2 μ m FATP‐1‐IN (HY‐141699, MedChemExpress) or 2 μ m Lipofermata (HY‐116788, MedChemExpress). ..

Article Title: Acidosis Forces Fatty Acid Uptake and Metabolism in Cancer Cells Regardless of Genotype.
Article Snippet: [26] Similarly, LD quantification was performed in bovine aortic endothelial cells and cardiomyocytes cultured in either 21% or 1% O2 conditions (H35 Hypoxystation, Don Whitley Scientific). .. For live cell BODIPY staining, 20 000 7.4> cancer cells were seeded in μslide 8 well high (80 806, Ibidi) and treated the day after with 7.4 or 6.5 pH medium containing 50 μm DHA in combination or not with 2 μg mL−1 JC63.1 (ab23680; Abcam), 10 μm SSO (SML2148, Merck), 2 μm FATP-1-IN (HY-141699, MedChemExpress) or 2 μm Lipofermata (HY-116788, MedChemExpress). ..

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( A and B ) FATP2 and loading control GAPDH mRNA expression was determined in human and mouse pancreatic tissue and α cell lines by RT-PCR (as described in Methods). Data are representative of 3 experiments per condition. ( C ) Mouse αTC1-6 cells were preincubated with lipofermata (1 hour, 37°C, 0–50 μM) in triplicate. BODIPY-labeled fatty acid uptake velocity was then determined, as described in Methods. Results show the mean ± SEM of 4 experiments.

Journal: The Journal of Clinical Investigation

Article Title: Fatty acid transport protein 2 inhibition enhances glucose tolerance through α cell–mediated GLP-1 secretion

doi: 10.1172/JCI192011

Figure Lengend Snippet: ( A and B ) FATP2 and loading control GAPDH mRNA expression was determined in human and mouse pancreatic tissue and α cell lines by RT-PCR (as described in Methods). Data are representative of 3 experiments per condition. ( C ) Mouse αTC1-6 cells were preincubated with lipofermata (1 hour, 37°C, 0–50 μM) in triplicate. BODIPY-labeled fatty acid uptake velocity was then determined, as described in Methods. Results show the mean ± SEM of 4 experiments.

Article Snippet: Wells were washed with serum-free, phenol-free media for 2 hours at 37° C. Lipofermata (5-bromo-5′-phenylspiro[3 H -1,3,4-thiadiazole-2,3′-indoline]-2-1) (MedChemExpress) was robotically incubated for the final hour.

Techniques: Control, Expressing, Reverse Transcription Polymerase Chain Reaction, Labeling

( A ) Pancreatic GLP-1 + α cell mass was determined as described in Methods in db/db and FATP2-KO db/db mice. * P < 0.01 compared with the db/db group by t test. ( B ) Human islets were preincubated with or without lipofermata (LF) and then tested for glucose-stimulated GLP-1 secretion as described in Methods. * P < 0.01 compared with all other groups by ANOVA. ( C ) αTC1-6 cells were preincubated with or without lipofermata or palmitate (Palm) as indicated. Glucose-stimulated GLP-1 secretion was then measured as described in Methods. Each symbol in the scatter bars in B and C represents 1 sample that was assayed in duplicate ( n = 3–6 samples per condition). * P < 0.05 compared lipofermata plus palmitate by ANOVA. ( D ) αTC1-6 cells coincubated in 5 mM or 25 mM glucose with or without 400 μM palmitate with or without 50 μM lipofermata for 16 hours were analyzed for Pcsk1 and Pcsk2 mRNA expression by qPCR. The results are expressed as the ratio relative to the 5 mM glucose-only condition. * P < 0.05 compared with other groups by ANOVA. ( E ) Glucose-stimulated insulin secretion was measured in human islets, which were preincubated with or without lipofermata and then exposed to exendin[9-39] (Ex) or palmitate, as described in Methods. Each symbol in the scatter bars represents 1 sample that was assayed in duplicate ( n = 3 samples per condition). * P < 0.01 compared with 16.8 mM glucose plus the lipofermata group by ANOVA. Data represent the mean ± SEM.

Journal: The Journal of Clinical Investigation

Article Title: Fatty acid transport protein 2 inhibition enhances glucose tolerance through α cell–mediated GLP-1 secretion

doi: 10.1172/JCI192011

Figure Lengend Snippet: ( A ) Pancreatic GLP-1 + α cell mass was determined as described in Methods in db/db and FATP2-KO db/db mice. * P < 0.01 compared with the db/db group by t test. ( B ) Human islets were preincubated with or without lipofermata (LF) and then tested for glucose-stimulated GLP-1 secretion as described in Methods. * P < 0.01 compared with all other groups by ANOVA. ( C ) αTC1-6 cells were preincubated with or without lipofermata or palmitate (Palm) as indicated. Glucose-stimulated GLP-1 secretion was then measured as described in Methods. Each symbol in the scatter bars in B and C represents 1 sample that was assayed in duplicate ( n = 3–6 samples per condition). * P < 0.05 compared lipofermata plus palmitate by ANOVA. ( D ) αTC1-6 cells coincubated in 5 mM or 25 mM glucose with or without 400 μM palmitate with or without 50 μM lipofermata for 16 hours were analyzed for Pcsk1 and Pcsk2 mRNA expression by qPCR. The results are expressed as the ratio relative to the 5 mM glucose-only condition. * P < 0.05 compared with other groups by ANOVA. ( E ) Glucose-stimulated insulin secretion was measured in human islets, which were preincubated with or without lipofermata and then exposed to exendin[9-39] (Ex) or palmitate, as described in Methods. Each symbol in the scatter bars represents 1 sample that was assayed in duplicate ( n = 3 samples per condition). * P < 0.01 compared with 16.8 mM glucose plus the lipofermata group by ANOVA. Data represent the mean ± SEM.

Techniques: Expressing

Yield of infectious HSV-1 and viral protein synthesis in BMDCs treated with inhibitors of lipid-metabolism-related enzymes Plaque-forming units (PFUs) and viral protein expression analyses (western blot) of HSV-1 late viral proteins (glycoprotein B, glycoprotein D, and VP16) in BMDCs treated for 3 h with the (A) DGAT1 inhibitor A-922500 (10 μM) (B) DGAT2 inhibitor PF-06424439 (10 μM), (C) ACAT inhibitor avasimibe (10 μM), (D) ACS inhibitor TOFA (10 μM), (E) ACS inhibitor triacsin C (10 μM), (F) lipase inhibitor CAY10499 (10 μM), (G) FATP inhibitor lipofermata (10 μM), or (H) CD36 inhibitor sulfosuccinimidyl oleate (SSO, 50 μM) and then infected with HSV-1 strain F at MOI 3 for 12 hpi or 18 hpi. (−) corresponds to vehicle treatment (DMSO) and (+) to treatment with the inhibitor. C + corresponds to Vero-HSV-1-infected cells (positive control). The analyses shown are means ± SEM of three independent assays. The statistical analyses were performed using two-way ANOVA and Bonferroni multiple comparisons test (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, ns: no statistical significance). See also <xref ref-type=

Figure S5 . " width="100%" height="100%">

Journal: iScience

Article Title: HSV-1 alters lipid metabolism and induces lipid droplet accumulation in functionally impaired mouse dendritic cells

doi: 10.1016/j.isci.2025.112441

Figure Lengend Snippet: Yield of infectious HSV-1 and viral protein synthesis in BMDCs treated with inhibitors of lipid-metabolism-related enzymes Plaque-forming units (PFUs) and viral protein expression analyses (western blot) of HSV-1 late viral proteins (glycoprotein B, glycoprotein D, and VP16) in BMDCs treated for 3 h with the (A) DGAT1 inhibitor A-922500 (10 μM) (B) DGAT2 inhibitor PF-06424439 (10 μM), (C) ACAT inhibitor avasimibe (10 μM), (D) ACS inhibitor TOFA (10 μM), (E) ACS inhibitor triacsin C (10 μM), (F) lipase inhibitor CAY10499 (10 μM), (G) FATP inhibitor lipofermata (10 μM), or (H) CD36 inhibitor sulfosuccinimidyl oleate (SSO, 50 μM) and then infected with HSV-1 strain F at MOI 3 for 12 hpi or 18 hpi. (−) corresponds to vehicle treatment (DMSO) and (+) to treatment with the inhibitor. C + corresponds to Vero-HSV-1-infected cells (positive control). The analyses shown are means ± SEM of three independent assays. The statistical analyses were performed using two-way ANOVA and Bonferroni multiple comparisons test (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, ns: no statistical significance). See also Figure S5 .

Article Snippet: Lipofermata , Cayman Chemical , Cat#25869; CAS No. 297180-15-5.

Techniques: Expressing, Western Blot, Infection, Positive Control

Inhibition of cholesterol ester synthesis (ACAT) or fatty acid uptake by fatty acid transport protein (FATP) recovers the viability of HSV-1-infected BMDCs Flow cytometry analyses of BMDC viability (determined as CD11c + /Zombie − cells) treated with (A) DGAT1 inhibitor A-922500 (10 μM), (B) DGAT2 inhibitor PF-06424439 (10 μM), (C) ACAT inhibitor avasimibe (10 μM), (D) ACS inhibitor TOFA (10 μM), (E) ACS inhibitor triacsin C (10 μM), (F) lipase inhibitor CAY10499 (10 μM), (G) FATP inhibitor lipofermata (10 μM), or (H) CD36 inhibitor sulfosuccinimidyl oleate (SSO, 50 μM) for 3 h, infected with HSV-1 strain F at MOI 3 for 1 h, and then further treated with the inhibitors for 17 h during infection. Vehicle treatment corresponds to the solvent used to dissolve the inhibitors (DMSO). The analyses shown are means ± SEM of three independent assays. The statistical analyses were performed using two-way ANOVA and Bonferroni multiple comparisons test (∗ p < 0.05, ∗∗ p < 0.01, ns: no statistical significance). See also <xref ref-type=

Figures S6 and . " width="100%" height="100%">

Journal: iScience

Article Title: HSV-1 alters lipid metabolism and induces lipid droplet accumulation in functionally impaired mouse dendritic cells

doi: 10.1016/j.isci.2025.112441

Figure Lengend Snippet: Inhibition of cholesterol ester synthesis (ACAT) or fatty acid uptake by fatty acid transport protein (FATP) recovers the viability of HSV-1-infected BMDCs Flow cytometry analyses of BMDC viability (determined as CD11c + /Zombie − cells) treated with (A) DGAT1 inhibitor A-922500 (10 μM), (B) DGAT2 inhibitor PF-06424439 (10 μM), (C) ACAT inhibitor avasimibe (10 μM), (D) ACS inhibitor TOFA (10 μM), (E) ACS inhibitor triacsin C (10 μM), (F) lipase inhibitor CAY10499 (10 μM), (G) FATP inhibitor lipofermata (10 μM), or (H) CD36 inhibitor sulfosuccinimidyl oleate (SSO, 50 μM) for 3 h, infected with HSV-1 strain F at MOI 3 for 1 h, and then further treated with the inhibitors for 17 h during infection. Vehicle treatment corresponds to the solvent used to dissolve the inhibitors (DMSO). The analyses shown are means ± SEM of three independent assays. The statistical analyses were performed using two-way ANOVA and Bonferroni multiple comparisons test (∗ p < 0.05, ∗∗ p < 0.01, ns: no statistical significance). See also Figures S6 and .

Article Snippet: Lipofermata , Cayman Chemical , Cat#25869; CAS No. 297180-15-5.

Techniques: Inhibition, Infection, Flow Cytometry, Solvent

Inhibition of ACAT in HSV-1-infected spleen DCs promotes enhanced migration of HSV-infected and non-infected DCs and the activation of the virus-specific CD8 + T cells in vivo (A) Schematic representation of the method used for assessing the migration of DCs to popliteal lymph nodes. DCs purified from the spleen were previously treated in vitro with the ACAT inhibitor avasimibe, FATP inhibitor lipofermata, or vehicle-treated for 3 h and then infected with HSV-1 strain F at MOI 3 for 6 h before injection into the footpads of mice. (B) Flow cytometry analyses of the migration of the DCs treated as indicated above with the ACAT inhibitor avasimibe (10 μM), FATP inhibitor lipofermata (10 μM), or vehicle-treated from the skin of footpads to popliteal lymph nodes 48 h after injection ( n = 3). (C) Schematic representation of the method used to assess skin-resident DC migration from the skin to popliteal lymph nodes (pLNs). Footpads were treated with ACAT inhibitor avasimibe (10 μM), FATP inhibitor lipofermata (10 μM), or vehicle for 1 h and then inoculated with HSV-1 strain F. (D) Flow cytometry analyses of total infiltrating DC migrating from the skin of footpads to popliteal lymph nodes 48 h after injection of the ACAT inhibitor avasimibe, FATP inhibitor lipofermata, or vehicle together with 1x10 6 PFU HSV-1 strain F in the footpad with the tracking dye CFSE (the analysis was performed over CFSE + /MHC-II + /CD11c + -gated cells). (E) Quantification of infiltrating dermal DCs (dDCs; CD207 + /CD103 + /MHC-II + /CD11c + /CFSE + cells) and (F) infiltrating Langerhans cells (LCs, CD207 + /CD103 − /MHC-II + /CD11c + /CFSE + cells) relocating from the skin to the draining popliteal lymph nodes after footpad injection of the ACAT inhibitor, FATP inhibitor, or vehicle and infection with HSV-1 and the tracking dye CFSE. (G) Surface expression of CD25 (T cell activation marker) in virus-specific gBT-I CD8 + T cells or (H) gDT-II CD4 + T cells obtained from popliteal lymph nodes of mice injected in the footpads with ACAT inhibitor avasimibe or FATP inhibitor lipofermata and then inoculated with HSV-1. A two-way ANOVA with the Bonferroni post-test was used. ( n = 3 mice/group, ∗ p < 0.05, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, ns: no statistical significance. See also <xref ref-type=

Figure S7 . " width="100%" height="100%">

Journal: iScience

Article Title: HSV-1 alters lipid metabolism and induces lipid droplet accumulation in functionally impaired mouse dendritic cells

doi: 10.1016/j.isci.2025.112441

Figure Lengend Snippet: Inhibition of ACAT in HSV-1-infected spleen DCs promotes enhanced migration of HSV-infected and non-infected DCs and the activation of the virus-specific CD8 + T cells in vivo (A) Schematic representation of the method used for assessing the migration of DCs to popliteal lymph nodes. DCs purified from the spleen were previously treated in vitro with the ACAT inhibitor avasimibe, FATP inhibitor lipofermata, or vehicle-treated for 3 h and then infected with HSV-1 strain F at MOI 3 for 6 h before injection into the footpads of mice. (B) Flow cytometry analyses of the migration of the DCs treated as indicated above with the ACAT inhibitor avasimibe (10 μM), FATP inhibitor lipofermata (10 μM), or vehicle-treated from the skin of footpads to popliteal lymph nodes 48 h after injection ( n = 3). (C) Schematic representation of the method used to assess skin-resident DC migration from the skin to popliteal lymph nodes (pLNs). Footpads were treated with ACAT inhibitor avasimibe (10 μM), FATP inhibitor lipofermata (10 μM), or vehicle for 1 h and then inoculated with HSV-1 strain F. (D) Flow cytometry analyses of total infiltrating DC migrating from the skin of footpads to popliteal lymph nodes 48 h after injection of the ACAT inhibitor avasimibe, FATP inhibitor lipofermata, or vehicle together with 1x10 6 PFU HSV-1 strain F in the footpad with the tracking dye CFSE (the analysis was performed over CFSE + /MHC-II + /CD11c + -gated cells). (E) Quantification of infiltrating dermal DCs (dDCs; CD207 + /CD103 + /MHC-II + /CD11c + /CFSE + cells) and (F) infiltrating Langerhans cells (LCs, CD207 + /CD103 − /MHC-II + /CD11c + /CFSE + cells) relocating from the skin to the draining popliteal lymph nodes after footpad injection of the ACAT inhibitor, FATP inhibitor, or vehicle and infection with HSV-1 and the tracking dye CFSE. (G) Surface expression of CD25 (T cell activation marker) in virus-specific gBT-I CD8 + T cells or (H) gDT-II CD4 + T cells obtained from popliteal lymph nodes of mice injected in the footpads with ACAT inhibitor avasimibe or FATP inhibitor lipofermata and then inoculated with HSV-1. A two-way ANOVA with the Bonferroni post-test was used. ( n = 3 mice/group, ∗ p < 0.05, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, ns: no statistical significance. See also Figure S7 .

Article Snippet: Lipofermata , Cayman Chemical , Cat#25869; CAS No. 297180-15-5.

Techniques: Inhibition, Infection, Migration, Activation Assay, Virus, In Vivo, Purification, In Vitro, Injection, Flow Cytometry, Expressing, Marker

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lipofermata (MedChemExpress)

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