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Selleck Chemicals vbit 12
Vbit 12, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 94/100, based on 17 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/vbit+12/VBIT-12/pmc12407563-59-0-1
Average 94 stars, based on 17 article reviews

vbit 12 - by Bioz Stars, 2026-10

94/100 stars

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Article Title: Voltage-dependent anion channel 1 oligomerization regulates PANoptosis in retinal ischemia–reperfusion injury
Article Snippet: VBIT-12 (Selleck, Houston, TX, USA, Cat#S8936) is a selective inhibitor of VDAC1 oligomerization (Niu et al., 2022).

Article Title: Targeting the Galectin‐7/ TRPM2 /Zn 2+ / DRP ‐1 Signaling Pathway: A Potential Therapeutic Intervention in the Pathogenesis of SJS / TEN
Article Snippet: Clotrimazole 10 (T0506, TargetMol), Mdivi-1 (HY-15886, MedChemExpress), VBIT-12 (#S8936), 11 cyclosporin A (#S2286), bromopyruvic acid (#S5426), TPEN (#S6962), and zinc 12 pyrithione (#S4075) were obtained from Selleck (Houston, TX, USA).

Article Title: VDAC1, as a downstream molecule of MLKL, participates in OGD/R-induced necroptosis by inducing mitochondrial damage
Article Snippet: VBIT-12 (Selleck, Cat#S8936) is a potent inhibitor of VDAC1, directly interacting with VDAC1 and interfering with its oligomerization [ , ].

Article Title: Phosphoglycerate mutase 5 aggravates alcoholic liver disease through disrupting VDAC-1-dependent mitochondrial integrity
Article Snippet: VBIT-12 (Selleck, #S8936, 10μm) was used to treat L02 cells 6 hours before EtOH treatment.

Article Title: The inhibition of VDAC1 oligomerization promotes pigmentation through the CaMK-CRTCs/CREB-MITF pathway.
Article Snippet: The voltage-dependent anion channel 1 (VDAC1) forms an oligomeric structure on the mitochondrial outer membrane, which plays critical roles in many physiological processes.. Research studies have demonstrated that the knockout of VDAC1 increases pigment content and up-regulates the expression of melanogenic genes.. Due to its involvement in various physiological processes, the depletion of VDAC1 has significant detrimental effects on cellular functions and the inhibition of VDAC1 oligomerization has recently emerged as a promising strategy for the treatment of several diseases.

Expressing:

Article Title: VDAC1-enriched apoptotic extracellular vesicles emerge as an autophagy activator orchestrating PDLSC-based bone regeneration
Article Snippet: Apoptosis is a programmed cell death process producing a large number of apoptotic extracellular vesicles (ApoEVs), which are involved in multiple pathophysiological states.. Periodontal ligament stem cell (PDLSC) transplantation is demonstrated to be an effective approach in bone regeneration, during which, PDLSCs undergo necessary apoptosis rather than differentiation into osteoblasts.. However, whether ApoEVs mediate PDLSC transplantation-based bone regeneration and the underlying mechanism remain largely unknown.

Modification:

Article Title: Mitochondria ATP Pro‐Ferroptosis by Adjusting the Conversion of PUFA to PUFA‐PLs
Article Snippet: .. See the T erm s and C onditions (https://onlinelibrary.w iley.com /term s-and-conditions) on W iley O nline L ibrary for rules of use; O A articles are governed by the applicable C reative C om m ons L icense (1397‐94‐0, MK), Bongkrekic acid (HY‐136406, MCE), SLV319 (HY‐121616, MCE), VBIT‐12 (S8936, Selleck), BODIPY‐C16 (D3821, ThermoFisher), Dulbecco's Modified Eagle's Medium high glucose (D0422‐100 mL, Sigma). ..

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The sequential events involved in the regulation of mtRNA release into the cytosol by IFN-α-100 and IC treatment. Stimulation of IFN-α-100 and ICs resulted in the release of calcium from the endoplasmic reticulum that entered the mitochondria, induced mitochondrial calcium overload, and triggered the opening of mitochondrial pores, including the oligomerization of voltage dependent anion channel (VDAC) and mPTP. The activation of adenine nucleotide translocase (ANT) also participated in the opening of mitochondrial pores in the inner mitochondrial membrane. Although ANT is not an essential component of the mPTP, ANT can regulate mPTP opening. The opening of the mPTP in the inner mitochondrial membrane and the oligomerization of VDAC1 resulted in the release of mtRNA into the cytosol, which activated its sensors RIG-I and MDA5 as well as several downstream inflammatory signaling pathways to induce innate immunity

Journal: Cell Communication and Signaling : CCS

Article Title: Interferon-alpha selectively signals mitochondrial pore opening to allow mitochondrial RNA release in systemic lupus erythematosus: pathophysiological implications

doi: 10.1186/s12964-026-02910-3

Figure Lengend Snippet: The sequential events involved in the regulation of mtRNA release into the cytosol by IFN-α-100 and IC treatment. Stimulation of IFN-α-100 and ICs resulted in the release of calcium from the endoplasmic reticulum that entered the mitochondria, induced mitochondrial calcium overload, and triggered the opening of mitochondrial pores, including the oligomerization of voltage dependent anion channel (VDAC) and mPTP. The activation of adenine nucleotide translocase (ANT) also participated in the opening of mitochondrial pores in the inner mitochondrial membrane. Although ANT is not an essential component of the mPTP, ANT can regulate mPTP opening. The opening of the mPTP in the inner mitochondrial membrane and the oligomerization of VDAC1 resulted in the release of mtRNA into the cytosol, which activated its sensors RIG-I and MDA5 as well as several downstream inflammatory signaling pathways to induce innate immunity

Article Snippet: Voltage-dependent anion channel oligomerization inhibitor (VBIT-12, HY-135885), endocytosis inhibitor (Pitstop 2, HY-115604; Dynasore, HY-15304), dynamin inhibitor, mitophagy inhibitor (Mdivi-1, HY-15886) and ethylene glycol bis(succinimidyl succinate) (EGS, HY-130458) were purchased from MedChemExpress LLC (Monmouth Junction, NJ, USA).

Techniques: Activation Assay, Membrane, Protein-Protein interactions

Representative western blots showing VDAC1 monomeric and dimeric forms, together with β-actin, in HCT116 cells pre-treated or not with the specific VDAC1 inhibitor VBIT12 (40 µM) for 2 h and then stimulated with rafoxanide (RFX, 2.5 μM) or DMSO (vehicle) for 5, 15, 30, and 60 min. One of 3 independent experiments in which similar results were obtained is shown.

Journal: Cell Death Discovery

Article Title: Rafoxanide disrupts mitochondrial homeostasis through VDAC1 modulation in colorectal cancer cells

doi: 10.1038/s41420-026-02986-3

Figure Lengend Snippet: Representative western blots showing VDAC1 monomeric and dimeric forms, together with β-actin, in HCT116 cells pre-treated or not with the specific VDAC1 inhibitor VBIT12 (40 µM) for 2 h and then stimulated with rafoxanide (RFX, 2.5 μM) or DMSO (vehicle) for 5, 15, 30, and 60 min. One of 3 independent experiments in which similar results were obtained is shown.

Article Snippet: HCT116 cells were pre-treated for 2 h with the VDAC1 inhibitor VBIT12 (40 μM, #S8936, Selleck Chemicals LLC, Houston, Texas) to block VDAC1 oligomerization or for 1 h with N-acetylcysteine (NAC, 1 mM, #A0150000, Sigma Aldrich) to decrease reactive oxygen species (ROS) level.

Techniques: Western Blot

$A Detection of total cellular reactive oxygen species (ROS) by fluorescence intensity measurement in HCT116 cells pre-treated or not with the ROS scavenger NAC (1 mM) for 1 h and then incubated with fluorescence probe DCFDA. After 30 min, cells were washed and stimulated with rafoxanide (RFX, 2.5 μM) or DMSO (vehicle). Fluorescence intensity was measured at the baseline and after 5, 15, 30, and 60 min upon stimulation. Differences among groups were compared using one-way analysis of variance (ANOVA) followed by the Tukey’s post hoc test (* P ≤ 0.05, ** P ≤ 0.01). One of 3 independent experiments where similar results were obtained. B Representative western blots showing VDAC1 monomeric and dimeric forms, together with β-actin, in HCT116 cells pre-treated or not with the ROS scavenger NAC (1 mM) for 1 h and then stimulated with rafoxanide (RFX, 2.5 μM) or DMSO (vehicle) for 1 h. One of 3 independent experiments in which similar results were obtained is shown. C Left panel : representative flow cytometry dot plots showing JC-1 fluorescence in HCT116 cells treated as indicated in panel ( B ). JC-1 aggregates indicate polarized mitochondria, whereas JC-1 monomers indicate mitochondrial membrane depolarization. Numbers indicate the percentage of cells in the designated quadrants. Right panel : quantification of the fraction of cells with depolarized mitochondria. Values are mean ± SEM of 3 independent experiments. Differences among groups were compared using one-way ANOVA followed by Tukey’s post hoc test (** P ≤ 0.01, *** P ≤ 0.001). D , E Complex I ( D ) and complex III ( E ) activity assays were performed spectrophotometrically in HCT116 cells stimulated with rafoxanide (RFX, 2.5 μM) or DMSO (vehicle) for 5 and 15 min. Values are mean ± SEM of 3 independent experiments. Differences among groups were compared using one-way ANOVA followed by Tukey’s post hoc test (* P ≤ 0.05, ** P ≤ 0.01). F Calcium mobilization was measured by flow cytometry in HCT116 cells stained with the 520-AM dye for 30 min, washed, and stimulated with rafoxanide (RFX, 2.5 μM), DMSO (vehicle), or ionomycin (positive control). Samples were acquired by flow cytometry at the baseline and immediately after stimulation. One of 3 independent experiments in which similar results were obtained is shown.$

Journal: Cell Death Discovery

Article Title: Rafoxanide disrupts mitochondrial homeostasis through VDAC1 modulation in colorectal cancer cells

doi: 10.1038/s41420-026-02986-3

Figure Lengend Snippet: A Detection of total cellular reactive oxygen species (ROS) by fluorescence intensity measurement in HCT116 cells pre-treated or not with the ROS scavenger NAC (1 mM) for 1 h and then incubated with fluorescence probe DCFDA. After 30 min, cells were washed and stimulated with rafoxanide (RFX, 2.5 μM) or DMSO (vehicle). Fluorescence intensity was measured at the baseline and after 5, 15, 30, and 60 min upon stimulation. Differences among groups were compared using one-way analysis of variance (ANOVA) followed by the Tukey’s post hoc test (* P ≤ 0.05, ** P ≤ 0.01). One of 3 independent experiments where similar results were obtained. B Representative western blots showing VDAC1 monomeric and dimeric forms, together with β-actin, in HCT116 cells pre-treated or not with the ROS scavenger NAC (1 mM) for 1 h and then stimulated with rafoxanide (RFX, 2.5 μM) or DMSO (vehicle) for 1 h. One of 3 independent experiments in which similar results were obtained is shown. C Left panel : representative flow cytometry dot plots showing JC-1 fluorescence in HCT116 cells treated as indicated in panel ( B ). JC-1 aggregates indicate polarized mitochondria, whereas JC-1 monomers indicate mitochondrial membrane depolarization. Numbers indicate the percentage of cells in the designated quadrants. Right panel : quantification of the fraction of cells with depolarized mitochondria. Values are mean ± SEM of 3 independent experiments. Differences among groups were compared using one-way ANOVA followed by Tukey’s post hoc test (** P ≤ 0.01, *** P ≤ 0.001). D , E Complex I ( D ) and complex III ( E ) activity assays were performed spectrophotometrically in HCT116 cells stimulated with rafoxanide (RFX, 2.5 μM) or DMSO (vehicle) for 5 and 15 min. Values are mean ± SEM of 3 independent experiments. Differences among groups were compared using one-way ANOVA followed by Tukey’s post hoc test (* P ≤ 0.05, ** P ≤ 0.01). F Calcium mobilization was measured by flow cytometry in HCT116 cells stained with the 520-AM dye for 30 min, washed, and stimulated with rafoxanide (RFX, 2.5 μM), DMSO (vehicle), or ionomycin (positive control). Samples were acquired by flow cytometry at the baseline and immediately after stimulation. One of 3 independent experiments in which similar results were obtained is shown.

Techniques: Fluorescence, Incubation, Western Blot, Flow Cytometry, Membrane, Activity Assay, Staining, Positive Control

VDAC1 inhibitor treatments significantly improves anemic hallmarks in adult Nan/+ mice. (A) Schematic diagram showing VDAC inhibitor (DMSO or VBIT4 or VBIT 12, 5 mg/kg) treatment. Oral gavage was used to introduce mice with DMSO (control) or VBIT4 or 12, and blood samples analyzed at various weeks as indicated (left top), followed by total harvest of bone marrow (BM) at the end for blood parameter. Quantification of RBC numbers (top middle), hematocrit (left bottom) and reticulocyte counts (right bottom). (B) Representative flow plot of BM cells isolated from DMSO or VBIT 4-treated mice and were analyzed for Ter119+ (left) and quantification (right). (C) Representative flow plot of bone marrow cells isolated from DMSO or VBIT 4-treated mice and were analyzed for red cell maturation and gated for G1-G5 as indicated (bottom), and quantification (bottom). (D) mitoROS analyzed in BM Ter119 + cells treated with DMSO or VBIT 4; histograms (left) and quantification (right) represented by Geo.mean. (E) MMP analyzed in BM Ter119 + cells treated with DMSO or VBIT 4; histograms (left) and quantification (right) represented by Geo.mean. (F) Serum IFN-α and -ß levels measured using ELISA in mice treated with DMSO or VBIT4. (G) Spleens were isolated from DMSO or VBIT4- or VBIT12-treated mice and weighed. Size is shown ( left ) and weight is quantified ( right ). Each experiment is an average (n=5). In all panels, data are presented as mean ± S.E.M. ( ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001, and ****p < 0.0001). (H) Model : Nan/+ fetal livers (E13.5) show ectopic and hypomorphic gene expression patterns due to the presence of the E339D variant. These cells are aberrantly enriched in L-carnitine and other metabolites. Their mitochondrial morphology is hyperfused and exhibit enhanced, but variable, degrees of disorganization, such as loss of cristae and detachment of inner membrane from outer membrane. Oligomerized VDAC1 mediates mtDNA release to the cytosol, which activates the mtDNA-cGAS-STING signaling pathway leading to increased transcripts for IFNs, interferon response genes (ISGs), and several inflammatory chemokine and cytokines. This mitochondrial dysregulation induces an inflammatory environment that inhibits proper erythroid maturation and causes ineffective erythropoiesis in Nan/+ embryos which persists into adulthood. Inhibition of the mtDNA-cGAS-STING module such as VDAC and STING with small molecules lowers the inflammatory response specifically in the Nan/+ erythroid cells and restores ineffective erythropoiesis seen in embryos fetal liver cells and in adults. (Model drawn via Biorender).

Journal: bioRxiv

Article Title: STING and VDAC inhibitors attenuate inflammation and ineffective erythropoiesis caused by an altered metabolome in the Nan (EKLF/E339D) mouse model of neonatal anemia

doi: 10.64898/2025.12.11.693792

Figure Lengend Snippet: VDAC1 inhibitor treatments significantly improves anemic hallmarks in adult Nan/+ mice. (A) Schematic diagram showing VDAC inhibitor (DMSO or VBIT4 or VBIT 12, 5 mg/kg) treatment. Oral gavage was used to introduce mice with DMSO (control) or VBIT4 or 12, and blood samples analyzed at various weeks as indicated (left top), followed by total harvest of bone marrow (BM) at the end for blood parameter. Quantification of RBC numbers (top middle), hematocrit (left bottom) and reticulocyte counts (right bottom). (B) Representative flow plot of BM cells isolated from DMSO or VBIT 4-treated mice and were analyzed for Ter119+ (left) and quantification (right). (C) Representative flow plot of bone marrow cells isolated from DMSO or VBIT 4-treated mice and were analyzed for red cell maturation and gated for G1-G5 as indicated (bottom), and quantification (bottom). (D) mitoROS analyzed in BM Ter119 + cells treated with DMSO or VBIT 4; histograms (left) and quantification (right) represented by Geo.mean. (E) MMP analyzed in BM Ter119 + cells treated with DMSO or VBIT 4; histograms (left) and quantification (right) represented by Geo.mean. (F) Serum IFN-α and -ß levels measured using ELISA in mice treated with DMSO or VBIT4. (G) Spleens were isolated from DMSO or VBIT4- or VBIT12-treated mice and weighed. Size is shown ( left ) and weight is quantified ( right ). Each experiment is an average (n=5). In all panels, data are presented as mean ± S.E.M. ( ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001, and ****p < 0.0001). (H) Model : Nan/+ fetal livers (E13.5) show ectopic and hypomorphic gene expression patterns due to the presence of the E339D variant. These cells are aberrantly enriched in L-carnitine and other metabolites. Their mitochondrial morphology is hyperfused and exhibit enhanced, but variable, degrees of disorganization, such as loss of cristae and detachment of inner membrane from outer membrane. Oligomerized VDAC1 mediates mtDNA release to the cytosol, which activates the mtDNA-cGAS-STING signaling pathway leading to increased transcripts for IFNs, interferon response genes (ISGs), and several inflammatory chemokine and cytokines. This mitochondrial dysregulation induces an inflammatory environment that inhibits proper erythroid maturation and causes ineffective erythropoiesis in Nan/+ embryos which persists into adulthood. Inhibition of the mtDNA-cGAS-STING module such as VDAC and STING with small molecules lowers the inflammatory response specifically in the Nan/+ erythroid cells and restores ineffective erythropoiesis seen in embryos fetal liver cells and in adults. (Model drawn via Biorender).

Article Snippet: VBIT-4 and VBIT12 was obtained from Selleckchem.

Techniques: Introduce, Control, Isolation, Enzyme-linked Immunosorbent Assay, Gene Expression, Variant Assay, Membrane, Inhibition

The effectiveness of the VDAC1 inhibitor in combination with trametinib in A549 cells and xenograft models. A Apoptotic effects of different concentrations of VBIT-12 on A549 cells. B , C Apoptosis and proliferation effects of VBIT-12 (10 µM) combined with trametinib (0.02 µM) on A549 cells. D Nude mice (n = 5) with xenograft tumors by injecting subcutaneously A549 cells (5 × 10 6 cells/0.1 mL) were treated with saline, VBIT-12 (10 mg/kg), trametinib (0.2 mg/kg), trametinib (0.2 mg/kg) + VBIT-12 (10 mg/kg) respectively, over a period of 14 days. E , F The last tumor volume ( E ) and mean tumor weight ( F ) (n = 5). Significant difference in the unpaired t-test with * p < 0.05 and ** p < 0.01, *** p < 0.001,**** p < 0.0001, ns = not significant

Journal: Discover Oncology

Article Title: VDAC1 as prognostic marker and therapeutic target in lung adenocarcinoma: a study integrating bioinformatics and experimental validation

doi: 10.1007/s12672-025-03955-5

Figure Lengend Snippet: The effectiveness of the VDAC1 inhibitor in combination with trametinib in A549 cells and xenograft models. A Apoptotic effects of different concentrations of VBIT-12 on A549 cells. B , C Apoptosis and proliferation effects of VBIT-12 (10 µM) combined with trametinib (0.02 µM) on A549 cells. D Nude mice (n = 5) with xenograft tumors by injecting subcutaneously A549 cells (5 × 10 6 cells/0.1 mL) were treated with saline, VBIT-12 (10 mg/kg), trametinib (0.2 mg/kg), trametinib (0.2 mg/kg) + VBIT-12 (10 mg/kg) respectively, over a period of 14 days. E , F The last tumor volume ( E ) and mean tumor weight ( F ) (n = 5). Significant difference in the unpaired t-test with * p < 0.05 and ** p < 0.01, *** p < 0.001,**** p < 0.0001, ns = not significant

Article Snippet: Trametinib and VBIT-12 (purchased from MedChemExpress, Shanghai) were prepared as DMSO stock solutions and serially diluted to working concentrations prior to experimentation.

Techniques: Saline