vbit-4 Search Results


94
TargetMol vbit 4
OGG1 inhibition promotes ferroptosis via an mPTP‐dependent mechanism. (A) NCI‐H1299 cells were treated with increased doses of RSL3 as indicated in the presence of TH5487 (5 µ m ) and Fer‐1 (2 µ m ) for 8 h; then cell survival rate was measured by Cell Titer Glo Viability Assay. (B) The morphology of NCI‐H1299 cells treated with RSL3 (0.5 µ m ) for 4 h following TH5487 (5 µ m ) and Fer‐1 (2 µ m ) pre‐treatment. Scale bar was 50 µm. (C) NCI‐H1299 were treated with 5 µ m erastin as indicated in the presence of TH5487 (5 µ m ) and Ferrostatin (Fer‐1, 2 µ m ) for 18 h, and the lipid peroxidation level was determined using C11‐BODIPY staining by flow cytometry. (D) Quantitative analysis of the fold change of lipid oxidation ratio in (C). (E) GPX4 siRNA were transfected to HT‐1080 cells, after 36 h, TH5487, SU0268 and Fer‐1 were added as indicated, then cells viability was detected using Cell Titer Glo. (F) NCI‐H1299 were treated with increased doses of erastin as indicated in the presence of TH5487 (5 µ m ), with or <t>without</t> <t>VBIT‐4</t> (5 µ m ) pretreatment for 8 h, then cell survival rate was measured by Cell Titer Glo Viability Assay. (G) NCI‐H1299 cells were treated with increased doses of erastin as indicated in the presence of TH5487 (5 µ m ), with or without CsA (5 µ m ) pretreatment for 24 h, and then the cell survival rate was measured by Cell Titer Glo Viability Assay. (H) CypD were knocked out in NCI‐H1299 cells, then the cells were treated with increased doses of erastin with or without TH5487 (5 µ m ) pretreatment. Cell death was measured by Cell Titer Glo Viability Assay. (I, J) ANT2 (I) and ANT3(J) were knocked down by specific siRNA in NCI‐H1299 cells, then the cells were treated with increased doses of erastin with or without TH5487 (5 µ m ) pretreatment. Cell death was measured by Cell Titer Glo Viability Assay. The statistical significance between different groups (D and E) was analyzed by Two‐Way ANOVA (Prism; GraphPad).
Vbit 4, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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94
MedChemExpress vdac
OGG1 inhibition promotes ferroptosis via an mPTP‐dependent mechanism. (A) NCI‐H1299 cells were treated with increased doses of RSL3 as indicated in the presence of TH5487 (5 µ m ) and Fer‐1 (2 µ m ) for 8 h; then cell survival rate was measured by Cell Titer Glo Viability Assay. (B) The morphology of NCI‐H1299 cells treated with RSL3 (0.5 µ m ) for 4 h following TH5487 (5 µ m ) and Fer‐1 (2 µ m ) pre‐treatment. Scale bar was 50 µm. (C) NCI‐H1299 were treated with 5 µ m erastin as indicated in the presence of TH5487 (5 µ m ) and Ferrostatin (Fer‐1, 2 µ m ) for 18 h, and the lipid peroxidation level was determined using C11‐BODIPY staining by flow cytometry. (D) Quantitative analysis of the fold change of lipid oxidation ratio in (C). (E) GPX4 siRNA were transfected to HT‐1080 cells, after 36 h, TH5487, SU0268 and Fer‐1 were added as indicated, then cells viability was detected using Cell Titer Glo. (F) NCI‐H1299 were treated with increased doses of erastin as indicated in the presence of TH5487 (5 µ m ), with or <t>without</t> <t>VBIT‐4</t> (5 µ m ) pretreatment for 8 h, then cell survival rate was measured by Cell Titer Glo Viability Assay. (G) NCI‐H1299 cells were treated with increased doses of erastin as indicated in the presence of TH5487 (5 µ m ), with or without CsA (5 µ m ) pretreatment for 24 h, and then the cell survival rate was measured by Cell Titer Glo Viability Assay. (H) CypD were knocked out in NCI‐H1299 cells, then the cells were treated with increased doses of erastin with or without TH5487 (5 µ m ) pretreatment. Cell death was measured by Cell Titer Glo Viability Assay. (I, J) ANT2 (I) and ANT3(J) were knocked down by specific siRNA in NCI‐H1299 cells, then the cells were treated with increased doses of erastin with or without TH5487 (5 µ m ) pretreatment. Cell death was measured by Cell Titer Glo Viability Assay. The statistical significance between different groups (D and E) was analyzed by Two‐Way ANOVA (Prism; GraphPad).
Vdac, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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86
Ambeed Inc b0579 vbit4 medchem express cat
OGG1 inhibition promotes ferroptosis via an mPTP‐dependent mechanism. (A) NCI‐H1299 cells were treated with increased doses of RSL3 as indicated in the presence of TH5487 (5 µ m ) and Fer‐1 (2 µ m ) for 8 h; then cell survival rate was measured by Cell Titer Glo Viability Assay. (B) The morphology of NCI‐H1299 cells treated with RSL3 (0.5 µ m ) for 4 h following TH5487 (5 µ m ) and Fer‐1 (2 µ m ) pre‐treatment. Scale bar was 50 µm. (C) NCI‐H1299 were treated with 5 µ m erastin as indicated in the presence of TH5487 (5 µ m ) and Ferrostatin (Fer‐1, 2 µ m ) for 18 h, and the lipid peroxidation level was determined using C11‐BODIPY staining by flow cytometry. (D) Quantitative analysis of the fold change of lipid oxidation ratio in (C). (E) GPX4 siRNA were transfected to HT‐1080 cells, after 36 h, TH5487, SU0268 and Fer‐1 were added as indicated, then cells viability was detected using Cell Titer Glo. (F) NCI‐H1299 were treated with increased doses of erastin as indicated in the presence of TH5487 (5 µ m ), with or <t>without</t> <t>VBIT‐4</t> (5 µ m ) pretreatment for 8 h, then cell survival rate was measured by Cell Titer Glo Viability Assay. (G) NCI‐H1299 cells were treated with increased doses of erastin as indicated in the presence of TH5487 (5 µ m ), with or without CsA (5 µ m ) pretreatment for 24 h, and then the cell survival rate was measured by Cell Titer Glo Viability Assay. (H) CypD were knocked out in NCI‐H1299 cells, then the cells were treated with increased doses of erastin with or without TH5487 (5 µ m ) pretreatment. Cell death was measured by Cell Titer Glo Viability Assay. (I, J) ANT2 (I) and ANT3(J) were knocked down by specific siRNA in NCI‐H1299 cells, then the cells were treated with increased doses of erastin with or without TH5487 (5 µ m ) pretreatment. Cell death was measured by Cell Titer Glo Viability Assay. The statistical significance between different groups (D and E) was analyzed by Two‐Way ANOVA (Prism; GraphPad).
B0579 Vbit4 Medchem Express Cat, supplied by Ambeed Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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86
Heumann Pharma aβ such as the vbit 4 peptide
OGG1 inhibition promotes ferroptosis via an mPTP‐dependent mechanism. (A) NCI‐H1299 cells were treated with increased doses of RSL3 as indicated in the presence of TH5487 (5 µ m ) and Fer‐1 (2 µ m ) for 8 h; then cell survival rate was measured by Cell Titer Glo Viability Assay. (B) The morphology of NCI‐H1299 cells treated with RSL3 (0.5 µ m ) for 4 h following TH5487 (5 µ m ) and Fer‐1 (2 µ m ) pre‐treatment. Scale bar was 50 µm. (C) NCI‐H1299 were treated with 5 µ m erastin as indicated in the presence of TH5487 (5 µ m ) and Ferrostatin (Fer‐1, 2 µ m ) for 18 h, and the lipid peroxidation level was determined using C11‐BODIPY staining by flow cytometry. (D) Quantitative analysis of the fold change of lipid oxidation ratio in (C). (E) GPX4 siRNA were transfected to HT‐1080 cells, after 36 h, TH5487, SU0268 and Fer‐1 were added as indicated, then cells viability was detected using Cell Titer Glo. (F) NCI‐H1299 were treated with increased doses of erastin as indicated in the presence of TH5487 (5 µ m ), with or <t>without</t> <t>VBIT‐4</t> (5 µ m ) pretreatment for 8 h, then cell survival rate was measured by Cell Titer Glo Viability Assay. (G) NCI‐H1299 cells were treated with increased doses of erastin as indicated in the presence of TH5487 (5 µ m ), with or without CsA (5 µ m ) pretreatment for 24 h, and then the cell survival rate was measured by Cell Titer Glo Viability Assay. (H) CypD were knocked out in NCI‐H1299 cells, then the cells were treated with increased doses of erastin with or without TH5487 (5 µ m ) pretreatment. Cell death was measured by Cell Titer Glo Viability Assay. (I, J) ANT2 (I) and ANT3(J) were knocked down by specific siRNA in NCI‐H1299 cells, then the cells were treated with increased doses of erastin with or without TH5487 (5 µ m ) pretreatment. Cell death was measured by Cell Titer Glo Viability Assay. The statistical significance between different groups (D and E) was analyzed by Two‐Way ANOVA (Prism; GraphPad).
Aβ Such As The Vbit 4 Peptide, supplied by Heumann Pharma, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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N/A
VBIT-4(CAT: I037979) is a selective inhibitor of voltage-dependent anion channel 1 (VDAC1) oligomerization with a binding affinity (Kd) of 17 μM. By targeting the mitochondrial protein VDAC1, it suppresses apoptosis and protects against mitochondrial dysfunction.
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InformationVBIT-4 VBIT-4 is a voltage-dependent anion channel (VDAC) oligomerization inhibitor that decreases mitochondrial DNA (mtDNA) release, type I interferon (IFN) signaling, neutrophil extracellular traps, and disease severity in a mouse model of systemic lupus erythematosus.TargetsVDAC
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OGG1 inhibition promotes ferroptosis via an mPTP‐dependent mechanism. (A) NCI‐H1299 cells were treated with increased doses of RSL3 as indicated in the presence of TH5487 (5 µ m ) and Fer‐1 (2 µ m ) for 8 h; then cell survival rate was measured by Cell Titer Glo Viability Assay. (B) The morphology of NCI‐H1299 cells treated with RSL3 (0.5 µ m ) for 4 h following TH5487 (5 µ m ) and Fer‐1 (2 µ m ) pre‐treatment. Scale bar was 50 µm. (C) NCI‐H1299 were treated with 5 µ m erastin as indicated in the presence of TH5487 (5 µ m ) and Ferrostatin (Fer‐1, 2 µ m ) for 18 h, and the lipid peroxidation level was determined using C11‐BODIPY staining by flow cytometry. (D) Quantitative analysis of the fold change of lipid oxidation ratio in (C). (E) GPX4 siRNA were transfected to HT‐1080 cells, after 36 h, TH5487, SU0268 and Fer‐1 were added as indicated, then cells viability was detected using Cell Titer Glo. (F) NCI‐H1299 were treated with increased doses of erastin as indicated in the presence of TH5487 (5 µ m ), with or without VBIT‐4 (5 µ m ) pretreatment for 8 h, then cell survival rate was measured by Cell Titer Glo Viability Assay. (G) NCI‐H1299 cells were treated with increased doses of erastin as indicated in the presence of TH5487 (5 µ m ), with or without CsA (5 µ m ) pretreatment for 24 h, and then the cell survival rate was measured by Cell Titer Glo Viability Assay. (H) CypD were knocked out in NCI‐H1299 cells, then the cells were treated with increased doses of erastin with or without TH5487 (5 µ m ) pretreatment. Cell death was measured by Cell Titer Glo Viability Assay. (I, J) ANT2 (I) and ANT3(J) were knocked down by specific siRNA in NCI‐H1299 cells, then the cells were treated with increased doses of erastin with or without TH5487 (5 µ m ) pretreatment. Cell death was measured by Cell Titer Glo Viability Assay. The statistical significance between different groups (D and E) was analyzed by Two‐Way ANOVA (Prism; GraphPad).

Journal: Advanced Science

Article Title: CypD Dependent mPTP Opening Is Crucial for Oxidized Mitochondrial DNA Release in Ferroptosis

doi: 10.1002/advs.202502239

Figure Lengend Snippet: OGG1 inhibition promotes ferroptosis via an mPTP‐dependent mechanism. (A) NCI‐H1299 cells were treated with increased doses of RSL3 as indicated in the presence of TH5487 (5 µ m ) and Fer‐1 (2 µ m ) for 8 h; then cell survival rate was measured by Cell Titer Glo Viability Assay. (B) The morphology of NCI‐H1299 cells treated with RSL3 (0.5 µ m ) for 4 h following TH5487 (5 µ m ) and Fer‐1 (2 µ m ) pre‐treatment. Scale bar was 50 µm. (C) NCI‐H1299 were treated with 5 µ m erastin as indicated in the presence of TH5487 (5 µ m ) and Ferrostatin (Fer‐1, 2 µ m ) for 18 h, and the lipid peroxidation level was determined using C11‐BODIPY staining by flow cytometry. (D) Quantitative analysis of the fold change of lipid oxidation ratio in (C). (E) GPX4 siRNA were transfected to HT‐1080 cells, after 36 h, TH5487, SU0268 and Fer‐1 were added as indicated, then cells viability was detected using Cell Titer Glo. (F) NCI‐H1299 were treated with increased doses of erastin as indicated in the presence of TH5487 (5 µ m ), with or without VBIT‐4 (5 µ m ) pretreatment for 8 h, then cell survival rate was measured by Cell Titer Glo Viability Assay. (G) NCI‐H1299 cells were treated with increased doses of erastin as indicated in the presence of TH5487 (5 µ m ), with or without CsA (5 µ m ) pretreatment for 24 h, and then the cell survival rate was measured by Cell Titer Glo Viability Assay. (H) CypD were knocked out in NCI‐H1299 cells, then the cells were treated with increased doses of erastin with or without TH5487 (5 µ m ) pretreatment. Cell death was measured by Cell Titer Glo Viability Assay. (I, J) ANT2 (I) and ANT3(J) were knocked down by specific siRNA in NCI‐H1299 cells, then the cells were treated with increased doses of erastin with or without TH5487 (5 µ m ) pretreatment. Cell death was measured by Cell Titer Glo Viability Assay. The statistical significance between different groups (D and E) was analyzed by Two‐Way ANOVA (Prism; GraphPad).

Article Snippet: RSL3 (T3646), erastin (T1765), ML210 (T8375), FINO2 ( T60084 ), CsA (T0945), DFO (T124358), BSO (T5471), TH5487 (T8119), SU0268 (T9119), Fer‐1 (T6500), VBIT‐4 ( T13287 ), H‐151 (T5674) and RU.521 (T5486) were ordered from TargetMol; Arachidonic acid (HY‐109590), Ardenic acid (HY‐W013215), and NIM811 (HY‐P0025) was purchased from MedChemExpress; IKE (MC2024) was purchased from MeilunBio.

Techniques: Inhibition, Viability Assay, Staining, Flow Cytometry, Transfection