2. Membrane Transporter/Ion Channel
  3. Potassium Channel
  4. DABMA

DABMA is a TMEM175 channel activator with a human EC50 of 17.9 μM. DABMA directly increases TMEM175 channel current via interaction with intracellular, transmembrane, or endosomal lumen-associated domains, and does not alter TMEM175 mRNA or protein levels. DABMA delays endolysosomal substrate degradation, modulates endolysosomal trafficking, increases acidic organelle accumulation, induces cholesterol accumulation and altered late endosome morphology. DABMA can be used for the research of coronavirus disease, Clostridium difficile infection, Pseudomonas aeruginosa infection, rabies, and influenza virus infection.

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DABMA

DABMA Chemical Structure

CAS No. : 893603-33-3

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DABMA Related Antibodies

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Description

DABMA is a TMEM175 channel activator with a human EC50 of 17.9 μM. DABMA directly increases TMEM175 channel current via interaction with intracellular, transmembrane, or endosomal lumen-associated domains, and does not alter TMEM175 mRNA or protein levels. DABMA delays endolysosomal substrate degradation, modulates endolysosomal trafficking, increases acidic organelle accumulation, induces cholesterol accumulation and altered late endosome morphology. DABMA can be used for the research of coronavirus disease, Clostridium difficile infection, Pseudomonas aeruginosa infection, rabies, and influenza virus infection[1][2][3].

In Vitro

DABMA (Compound 3j) (2 h pre-infection, 48 h post-infection) inhibits SARS-CoV-2 infection in Vero E6 cells with an IC50 of 4.9 μM[1].
DABMA (2 h pre-infection, 20 h post-infection) inhibits SARS-CoV-2 infection in U2OS-ACE2 cells with an IC50 of 3.3 μM[1].
DABMA (5 min bath solution) directly activates hTMEM175 channels in isolated endosomes from HEK293T cells with an EC50 of 17.9 μM, acting via extracellular/cytosolic or transmembrane domains without altering channel expression levels[1].
DABMA (15-30 μM; 20 h) has protective activity against diphtheria toxin (DT) cytotoxicity in A549 cells that is significantly attenuated by TMEM175 depletion, with protection factors decreasing from 6.2 to 3.5 at 15 μM and from 75.7 to 28.8 at 30 μM[1].
DABMA (30 μM; 24 h) has protective activity against toxin B from Clostridium difficile (TcsL)-induced cell rounding in Vero cells that is significantly attenuated by TMEM175 depletion, reducing cell rounding to only 83.0% in knockdown cells compared to 54.6% in control cells[1].
DABMA (30 μM; 5 h) delays endolysosomal degradation of DQ-BSA (HY-D2449), an ability that is significantly attenuated by TMEM175 depletion, reducing the compound's inhibitory effect by approximately 40% compared to control cells[1].
DABMA (30 μM; 6 h) significantly increases LysoTracker Green fluorescence intensity in TMEM175 WT HeLa cells, but this effect is completely abolished in TMEM175 KO HeLa cells, with no impact on mitochondrial staining in either cell type[1].
DABMA (30 μM; 6 h) significantly increases Rab7 signal intensity in TMEM175 WT HeLa cells, but this effect is abolished in TMEM175 KO HeLa cells where basal Rab7 levels are already elevated[1].
DABMA potently inhibits DT-induced cytotoxicity in A549 cells with an EC50 of 25.7 μM[2].
DABMA (30-60 μM) exhibits low long-term toxicity in A549 cells, with a CC50 of 119.7 μM and no reduction in cell viability or colony formation[2].
DABMA inhibits DT-induced cytotoxicity in Vero, PC3, A431, DLD1, and primary HUVEC cells with consistent activity, demonstrating non-cell-type-specific efficacy[2].
DABMA (30 μM; 2 h) alters acidic endosome morphology and increases Lysotracker Deep Red staining intensity in A549 cells, indicating perturbation of endolysosomal function[2].
DABMA (30 μM; 18 h) induces intracellular cholesterol accumulation in A549 cells, as shown by increased Filipin III staining intensity[2].
DABMA (30 μM; 6 h) targets late endosomes in A549 cells, as shown by increased Rab7 immunostaining intensity[2].
DABMA (15 μM) acts synergistically with Baf A1 to protect A549 cells against DT-induced cytotoxicity, producing a combined protection factor of over 300 without additive toxicity[2].
DABMA (30 μM; 4 h) inhibits TcdB-induced cell rounding in Vero cells with an EC50 of 38.6 μM and a selectivity index of 6.34[2].
DABMA (30 μM; 16 h) inhibits TcsL-induced cell rounding in Vero cells with an EC50 of 15.8 μM and a selectivity index of 7.38[2].
DABMA (30 μM; 18 h) inhibits PE-induced cytotoxicity in L929 cells with an EC50 of 20.77 μM and a selectivity index of 4.35[2].
DABMA (1-40 μM; 28 h) potently inhibits RABV infection in BSR cells[2].
DABMA (0.1-10 μM; 25 h) potently inhibits EBOV infection in HeLa cells with an EC50 of 908 nM, a CC50 of 116.7 μM, and a selectivity index greater than 120[2].
DABMA (range; 72 h) exhibits cytotoxicity in MDCK cells with a CC50 of 42.71 µM and in A549 cells with a CC50 of 47.42 µM[3].
DABMA (5 h pre-incubation) potently inhibits influenza virus-induced CPE in MDCK cells with EC50 values ranging from 1.82 µM to 6.73 µM across amantadine-sensitive, amantadine-resistant, and influenza B virus strains[3].
DABMA (3.75-15 µM; 5 h pre-incubation) dose-dependently reduces viral titers of A/NY/61/LV16A (H1N1) and A/17/HK/2014/8296 (H3N2) in MDCK and A549 cells after 5 h pre-incubation and 48 h of infection, with significant reductions observed at 3.75, 7.5, and 15 µM[3].
DABMA (15 µM; 5 h pre-incubation) inhibits H1N1 (A/NY/61/LV16A) genomic RNA replication by 86.51% and reduces NP synthesis in MDCK cells, and significantly decreases NP fluorescence intensity in infected A549 cells after 5 h pre-incubation and 16 h of infection[3].
DABMA (15 µM) impairs early stages of H1N1 (A/NY/61/LV16A) infection in MDCK cells by inhibiting viral entry, without affecting virus binding to cells[3].

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

DABMA Related Antibodies

Cell Cytotoxicity Assay[1]

Cell Line: scrambled shRNA control A549 cells, TMEM175-knockdown (shTMEM175) A549 cells
Concentration: 15 μM; 30 μM
Incubation Time: 20 h
Result: Reversed DT-induced protein synthesis inhibition in scrambled control A549 cells with a protection factor of 6.2 at 15 μM.
Reversed DT-induced protein synthesis inhibition in scrambled control A549 cells with a protection factor of 75.7 at 30 μM.
Showed significantly reduced protection factor of 3.5 at 15 μM in shTMEM175 A549 cells.
Showed significantly reduced protection factor of 28.8 at 30 μM in shTMEM175 A549 cells.

Cell Cytotoxicity Assay[1]

Cell Line: scrambled shRNA control Vero cells, TMEM175-knockdown (shTMEM175) Vero cells
Concentration: 30 μM
Incubation Time: 24 h
Result: Reduced TcsL-induced cell rounding from 96.7% to 54.6% in scrambled control Vero cells.
Showed significantly diminished protective effect in shTMEM175 Vero cells, with 83.0% of cells remaining rounded.

Immunofluorescence[2]

Cell Line: A549 cells
Concentration: 30 μM
Incubation Time: 6 h
Result: Significantly increased Rab7 fluorescence intensity compared to DMSO control, indicating expansion of late endosomes.

Cell Cytotoxicity Assay[2]

Cell Line: Vero cells
Concentration: 30 μM
Incubation Time: 4 h
Result: Reduced TcdB-induced cell rounding more efficiently than ABMA at 30 μM.
Had an EC50 of 38.6 μM against TcdB.
Showed a selectivity index of 6.34.

Cell Cytotoxicity Assay[2]

Cell Line: Vero cells
Concentration: 30 μM
Incubation Time: 16 h
Result: Inhibited TcsL-induced cell rounding with 5.6-fold greater efficacy than ABMA at 30 μM.
Had an EC50 of 15.8 μM against TcsL.
Showed a selectivity index of 7.38.

Cell Cytotoxicity Assay[2]

Cell Line: L929 cells
Concentration: 30 μM
Incubation Time: 18 h
Result: Protected against PE-induced protein synthesis reduction with 4.8-fold greater efficacy than ABMA at 30 μM.
Had an EC50 of 20.77 μM against PE.
Showed a selectivity index of 4.35.
In Vivo

DABMA (1.25-5 mg/kg; i.p.; daily; 6 days) confers 67% survival protection in H1N1-infected BALB/c mice, while significantly reducing lung viral load, lung index, and lung pathology[3].

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

Animal Model: BALB/c (female, 6-8 weeks old, specific pathogen-free)[3]
Dosage: 1.25 mg/kg; 5 mg/kg
Administration: i.p.; daily; 6 days
Result: Improved mouse survival rate to 67% compared to 0% in the placebo group.
Showed statistically significant higher body weights than the placebo group on days 5-8 post-inoculation.
Significantly reduced relative lung viral RNA load, lung index, and lung virus titer compared to the placebo group at 6 days post-inoculation.
Reduced influenza-induced lung histopathological lesions, including pulmonary septum thickening and inflammatory cell infiltration.
Showed no toxicity in uninfected mice.
Molecular Weight

378.35

Formula

C20H28BrNO
CAS No.
SMILES

BrC1=CC=C(C(CNC23CC4CC(C2)(CC(C4)(C3)C)C)=C1)OC
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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DABMA Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    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.

Keywords:

DABMA893603-33-3Potassium ChannelKcsAA549 cellsHeLa cellsH1N1U2OS-ACE2 cellsdiphtheria toxinClostridium sordelliiVero E6 cellsSARS-CoV-2HEK293T cellsTMEM175Inhibitorinhibitorinhibit

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