DABMA

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.