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a939572 t4515  (TargetMol)


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    TargetMol a939572 t4515
    VA analogues inhibit ferroptosis through the regulation of MUFA metabolism. (A, B) Lipidomic analysis of MUFAs and PUFAs in membrane lipids including PE (A) and PC (B) following VA (5 μmol/L) and D3 (5 μmol/L) treatment for 12 h in HT-1080 cells. (C) Viability HT-1080 cells treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L) or ATRA (10 μmol/L) in the presence or absence of SCD1 inhibitor <t>A939572</t> (20 μmol/L) for 24 h. (D) Validation of SCD1 KO in HT-1080 cells. (E) The levels of OA-CoA were decreased in SCD1 knockout HT-1080 cells. (F) Viability of Vector and SCD1 KO cells treated with RSL3 for 24 h. (G) SCD1 KO compromised the anti-ferroptotic effect of VA analogues in HT-1080 cells. Cells were treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. (H, I) Supplement of OA restored the protective effect of VA analogues against ferroptosis. Vector and SCD1 KO HT-1080 cells were pretreated with OA in (10 and 20 μmol/L in panel H, and 10 μmol/L in panel I, followed by treatment with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. All the data are presented as the mean ± SD ( n = 3). ∗ P < 0.05, ∗∗∗ P < 0.001, indicating significant differences between groups.
    A939572 T4515, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/a939572/pmc13031062-278-20-25?v=TargetMol
    Average 94 stars, based on 6 article reviews
    a939572 t4515 - by Bioz Stars, 2026-07
    94/100 stars

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    1) Product Images from "Vitamin A and its analogues modulate MUFAs metabolism to improve ferroptosis and aging by direct targeting of ACSL3"

    Article Title: Vitamin A and its analogues modulate MUFAs metabolism to improve ferroptosis and aging by direct targeting of ACSL3

    Journal: Acta Pharmaceutica Sinica. B

    doi: 10.1016/j.apsb.2025.11.004

    VA analogues inhibit ferroptosis through the regulation of MUFA metabolism. (A, B) Lipidomic analysis of MUFAs and PUFAs in membrane lipids including PE (A) and PC (B) following VA (5 μmol/L) and D3 (5 μmol/L) treatment for 12 h in HT-1080 cells. (C) Viability HT-1080 cells treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L) or ATRA (10 μmol/L) in the presence or absence of SCD1 inhibitor A939572 (20 μmol/L) for 24 h. (D) Validation of SCD1 KO in HT-1080 cells. (E) The levels of OA-CoA were decreased in SCD1 knockout HT-1080 cells. (F) Viability of Vector and SCD1 KO cells treated with RSL3 for 24 h. (G) SCD1 KO compromised the anti-ferroptotic effect of VA analogues in HT-1080 cells. Cells were treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. (H, I) Supplement of OA restored the protective effect of VA analogues against ferroptosis. Vector and SCD1 KO HT-1080 cells were pretreated with OA in (10 and 20 μmol/L in panel H, and 10 μmol/L in panel I, followed by treatment with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. All the data are presented as the mean ± SD ( n = 3). ∗ P < 0.05, ∗∗∗ P < 0.001, indicating significant differences between groups.
    Figure Legend Snippet: VA analogues inhibit ferroptosis through the regulation of MUFA metabolism. (A, B) Lipidomic analysis of MUFAs and PUFAs in membrane lipids including PE (A) and PC (B) following VA (5 μmol/L) and D3 (5 μmol/L) treatment for 12 h in HT-1080 cells. (C) Viability HT-1080 cells treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L) or ATRA (10 μmol/L) in the presence or absence of SCD1 inhibitor A939572 (20 μmol/L) for 24 h. (D) Validation of SCD1 KO in HT-1080 cells. (E) The levels of OA-CoA were decreased in SCD1 knockout HT-1080 cells. (F) Viability of Vector and SCD1 KO cells treated with RSL3 for 24 h. (G) SCD1 KO compromised the anti-ferroptotic effect of VA analogues in HT-1080 cells. Cells were treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. (H, I) Supplement of OA restored the protective effect of VA analogues against ferroptosis. Vector and SCD1 KO HT-1080 cells were pretreated with OA in (10 and 20 μmol/L in panel H, and 10 μmol/L in panel I, followed by treatment with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. All the data are presented as the mean ± SD ( n = 3). ∗ P < 0.05, ∗∗∗ P < 0.001, indicating significant differences between groups.

    Techniques Used: Analogues, Membrane, Biomarker Discovery, Knock-Out, Plasmid Preparation



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    VA analogues inhibit ferroptosis through the regulation of MUFA metabolism. (A, B) Lipidomic analysis of MUFAs and PUFAs in membrane lipids including PE (A) and PC (B) following VA (5 μmol/L) and D3 (5 μmol/L) treatment for 12 h in HT-1080 cells. (C) Viability HT-1080 cells treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L) or ATRA (10 μmol/L) in the presence or absence of SCD1 inhibitor <t>A939572</t> (20 μmol/L) for 24 h. (D) Validation of SCD1 KO in HT-1080 cells. (E) The levels of OA-CoA were decreased in SCD1 knockout HT-1080 cells. (F) Viability of Vector and SCD1 KO cells treated with RSL3 for 24 h. (G) SCD1 KO compromised the anti-ferroptotic effect of VA analogues in HT-1080 cells. Cells were treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. (H, I) Supplement of OA restored the protective effect of VA analogues against ferroptosis. Vector and SCD1 KO HT-1080 cells were pretreated with OA in (10 and 20 μmol/L in panel H, and 10 μmol/L in panel I, followed by treatment with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. All the data are presented as the mean ± SD ( n = 3). ∗ P < 0.05, ∗∗∗ P < 0.001, indicating significant differences between groups.
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    Image Search Results


    VA analogues inhibit ferroptosis through the regulation of MUFA metabolism. (A, B) Lipidomic analysis of MUFAs and PUFAs in membrane lipids including PE (A) and PC (B) following VA (5 μmol/L) and D3 (5 μmol/L) treatment for 12 h in HT-1080 cells. (C) Viability HT-1080 cells treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L) or ATRA (10 μmol/L) in the presence or absence of SCD1 inhibitor A939572 (20 μmol/L) for 24 h. (D) Validation of SCD1 KO in HT-1080 cells. (E) The levels of OA-CoA were decreased in SCD1 knockout HT-1080 cells. (F) Viability of Vector and SCD1 KO cells treated with RSL3 for 24 h. (G) SCD1 KO compromised the anti-ferroptotic effect of VA analogues in HT-1080 cells. Cells were treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. (H, I) Supplement of OA restored the protective effect of VA analogues against ferroptosis. Vector and SCD1 KO HT-1080 cells were pretreated with OA in (10 and 20 μmol/L in panel H, and 10 μmol/L in panel I, followed by treatment with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. All the data are presented as the mean ± SD ( n = 3). ∗ P < 0.05, ∗∗∗ P < 0.001, indicating significant differences between groups.

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: Vitamin A and its analogues modulate MUFAs metabolism to improve ferroptosis and aging by direct targeting of ACSL3

    doi: 10.1016/j.apsb.2025.11.004

    Figure Lengend Snippet: VA analogues inhibit ferroptosis through the regulation of MUFA metabolism. (A, B) Lipidomic analysis of MUFAs and PUFAs in membrane lipids including PE (A) and PC (B) following VA (5 μmol/L) and D3 (5 μmol/L) treatment for 12 h in HT-1080 cells. (C) Viability HT-1080 cells treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L) or ATRA (10 μmol/L) in the presence or absence of SCD1 inhibitor A939572 (20 μmol/L) for 24 h. (D) Validation of SCD1 KO in HT-1080 cells. (E) The levels of OA-CoA were decreased in SCD1 knockout HT-1080 cells. (F) Viability of Vector and SCD1 KO cells treated with RSL3 for 24 h. (G) SCD1 KO compromised the anti-ferroptotic effect of VA analogues in HT-1080 cells. Cells were treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. (H, I) Supplement of OA restored the protective effect of VA analogues against ferroptosis. Vector and SCD1 KO HT-1080 cells were pretreated with OA in (10 and 20 μmol/L in panel H, and 10 μmol/L in panel I, followed by treatment with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. All the data are presented as the mean ± SD ( n = 3). ∗ P < 0.05, ∗∗∗ P < 0.001, indicating significant differences between groups.

    Article Snippet: All- trans -retinal (T5256), Fenretinide (T1872), Acitretin (T1330), AGN193109 (TQ0097), HX531( T22843 ), Ch55 ( T14946 ), Adapalene (T1093) and A939572 (T4515) were purchased from TargetMOI (Shanghai, China).

    Techniques: Analogues, Membrane, Biomarker Discovery, Knock-Out, Plasmid Preparation