1. Membrane Transporter/Ion Channel Cell Cycle/DNA Damage
  2. VDAC RAD51
  3. DIDS

DIDS is a dual inhibitor of ABCA1 and VDAC1. DIDS also inhibits RAD51, inhibiting RAD51-mediated homologous pairing and strand exchange reactions. DIDS inhibits anion exchange and binding to red blood cell membranes, inhibits the activation of caspase-3 and -9, and can be used in cancer research.

For research use only. We do not sell to patients.

CAS No. : 53005-05-3

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Top Publications Citing Use of Products

    DIDS purchased from MedChemExpress. Usage Cited in: Cell Death Dis. 2024 Nov 9;15(11):811.  [Abstract]

    H1299 cells were transfected with GFP or GFP-VDAC1 for 18 h and subsequently treated with 100 μM NSC15364 or 400 μM DIDS for 12 h.

    DIDS purchased from MedChemExpress. Usage Cited in: Cell Death Dis. 2024 Nov 9;15(11):811.  [Abstract]

    H1299 cells were incubated in a control or cysteine-deprived medium with or without DIDS for the indicated concentration for 24 h.

    DIDS purchased from MedChemExpress. Usage Cited in: Cell Death Dis. 2024 Nov 9;15(11):811.  [Abstract]

    H1299 cells were incubated in a control or cysteine-deprived medium with or without 400 μM DIDS for 12 h.

    DIDS purchased from MedChemExpress. Usage Cited in: Cell Death Dis. 2024 Nov 9;15(11):811.  [Abstract]

    H1299 cells were incubated in a control or cysteine-deprived medium with or without 100 μM NSC15364 or 400 μM DIDS for 12 h. A representative fluorescence microscopy image of MitoSOX red staining. The green fluorescence of MitoBright LT green shows the location of mitochondria (scale bar = 100 μm).

    DIDS purchased from MedChemExpress. Usage Cited in: Autophagy. 2021 Nov;17(11):3592-3606.  [Abstract]

    Effect of DIDS (10 μM, 1 h-pretreatment) on CBD-induced glioma cell death. U251 or LN18 cells were pretreated with DIDS and then treated with CBD (30 μM) for 48 h. Cell viability was determined by the MTT assay.

    DIDS purchased from MedChemExpress. Usage Cited in: Adv Sci (Weinh). 2021 Nov;8(21):e2101936.  [Abstract]

    HCT116 cells were pretreated with DIDS (20 μM) for 1 h, followed by SR140333 treatment for 24 h.

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    Description

    DIDS is a dual inhibitor of ABCA1 and VDAC1. DIDS also inhibits RAD51, inhibiting RAD51-mediated homologous pairing and strand exchange reactions. DIDS inhibits anion exchange and binding to red blood cell membranes, inhibits the activation of caspase-3 and -9, and can be used in cancer research[1][2][3][4].

    IC50 & Target

    VDAC1

     

    Cellular Effect
    Cell Line Type Value Description References
    Erythrocyte IC50
    31 μM
    Compound: DIDS
    Inhibition of erythrocyte anion transport protein
    Inhibition of erythrocyte anion transport protein
    [PMID: 18078758]
    In Vitro

    DIDS (0-10 μM) inhibits RAD51-mediated strand exchange[1].
    DIDS (0-20 μM) inhibits DNA binding by RAD51[1].
    DIDS (10 μM; 0-60 min) stimulates the ATP hydrolyzing activity of RAD51 in the absence of DNA[1].
    DIDS (50-400 μM) prevents effect on ALA-SDT-induced cell death, while dose at 50 μM has no inhibition effect, and dose at 400 μM insifnificantly decreases the cell viability[2].
    DIDS (100 μM) clearly inhibits caspase-3 and caspase-9 activation[2].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    Molecular Weight

    454.52

    Formula

    C16H10N2O6S4

    CAS No.
    SMILES

    O=S(C1=CC(N=C=S)=CC=C1/C=C/C2=CC=C(C=C2S(=O)(O)=O)N=C=S)(O)=O

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage

    Please store the product under the recommended conditions in the Certificate of Analysis.

    Purity & Documentation
    References
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      Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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    Product Name:
    DIDS
    Cat. No.:
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