2. Stem Cell/Wnt TGF-beta/Smad Apoptosis Membrane Transporter/Ion Channel
  3. TGF-beta/Smad Apoptosis Chloride Channel
  4. Ammonium chloride, for molecular biology

Ammonium chloride, for molecular biology  (Synonyms: Salmiac, for molecular biology)

Cat. No.: HY-Y1269D
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Ammonium chloride (Salmiac), for molecular biology is an inhibitor of Slc26a4 and SMAD2. Ammonium chloride, for molecular biology reduces the protein expression level of Slc26a4 in lung tissue, and attenuates ozone-induced increases in proinflammatory cytokines, inflammatory cells, pulmonary resistance, goblet cell hyperplasia, peribronchial inflammation and thiocyanate levels in mouse tissues and bronchoalveolar lavage fluid. Ammonium chloride, for molecular biology decreases the level of phosphorylated SMAD2, inhibits autophagy by reducing autophagy-related proteins, and enhances Cisplatin (HY-17394)-induced cancer cell apoptosis and DNA double-strand breaks. Ammonium chloride, for molecular biology also inhibits the TCA cycle, reduces ATP production, increases glucose utilization, regulates the levels of lactic acid, glutamic acid and ATP, and induces morphological degeneration of neuroblastoma cells. Ammonium chloride, for molecular biology can be used in studies related to ozone-induced airway injury, hepatocellular carcinoma, human cervical cancer, hepatic encephalopathy, Reye syndrome, epilepsy and neurodegenerative diseases.

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CAS No. : 12125-02-9

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Ammonium chloride, for molecular biology Related Antibodies

Top Publications Citing Use of Products

47 Publications Citing Use of MCE Ammonium chloride, for molecular biology

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Bio/Physico-chemical Assay

    Ammonium chloride, for molecular biology purchased from MedChemExpress. Usage Cited in: Adv Sci (Weinh). 2025 Aug 4:e04680.  [Abstract]

    Resistant cells were treated with 25 mM Ammonium chloride (NH4Cl) alone or co‐treated with 80 µm FA, and the expression level of DDX6 was detected by immunoblotting, n = 3. The results showed that supplementation with the lysosomal inhibitor NH4Cl could rescue DDX6 expression reduced by FA intervention.

    Ammonium chloride, for molecular biology purchased from MedChemExpress. Usage Cited in: MedComm (2020). 2025 Aug 31;6(9):e70353.  [Abstract]

    HEK293T‐hACE2 cells were exposed to pseudotyped SARS‐COV‐2 (wild type and two variants: B.1.351 and B.1.671) or VSV (MOI = 10) in the presence of varying concentrations of tetrandrine or Ammonium chloride (NH4Cl). Firefly luciferase activity, indicative of infection, was measured 24 h post‐infection and normalized to the mock‐treated control. *p < 0.05, **p < 0.01, ***p < 0.001 versus virus control. Mock, cell group. Con, virus‐infected group.

    Ammonium chloride, for molecular biology purchased from MedChemExpress. Usage Cited in: Cancer Lett. 2025 Apr 10:217715.  [Abstract]

    Western blot was used to test the influence of Bufalin (100 nM) combined with Ammonium chloride (NH4CL, 30 mM) or BafA1 (50 nM) for different time (0, 0.5, 1, 2 h) in KYSE30 and KYSE450. The results showed that Bufalin-induced EGFR degradation could be reversed by lysosomal protease NH4CL.

    Ammonium chloride, for molecular biology purchased from MedChemExpress. Usage Cited in: Eur J Med Chem. 2025 Jun 14:296:117871.  [Abstract]

    Immunoblots and quantification of EGFR in A549 cells treated with different concentrations of LY-dE#5, with or without MG132, CQ, and Ammonium chloride (NH4Cl) (0.5-2 μM). The results showed that NH4Cl significantly blocked LY-dE#5-mediated EGFR degradation.

    Ammonium chloride, for molecular biology purchased from MedChemExpress. Usage Cited in: PLoS Pathog. 2025 Jul 16;21(7):e1013344.  [Abstract]

    293T cells were transfected with the pCAGGS-HA-ORF3a plasmid and subsequently treated with Ammonium chloride (NH4Cl) (20 mM). Cells were harvested after 48 h, and the expression levels of endogenous YY1 were assessed by Western blot using either HA or YY1 antibodies.

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    제품 설명

    Ammonium chloride (Salmiac), for molecular biology is an inhibitor of Slc26a4 and SMAD2. Ammonium chloride, for molecular biology reduces the protein expression level of Slc26a4 in lung tissue, and attenuates ozone-induced increases in proinflammatory cytokines, inflammatory cells, pulmonary resistance, goblet cell hyperplasia, peribronchial inflammation and thiocyanate levels in mouse tissues and bronchoalveolar lavage fluid. Ammonium chloride, for molecular biology decreases the level of phosphorylated SMAD2, inhibits autophagy by reducing autophagy-related proteins, and enhances Cisplatin (HY-17394)-induced cancer cell apoptosis and DNA double-strand breaks. Ammonium chloride, for molecular biology also inhibits the TCA cycle, reduces ATP production, increases glucose utilization, regulates the levels of lactic acid, glutamic acid and ATP, and induces morphological degeneration of neuroblastoma cells. Ammonium chloride, for molecular biology can be used in studies related to ozone-induced airway injury, hepatocellular carcinoma, human cervical cancer, hepatic encephalopathy, Reye syndrome, epilepsy and neurodegenerative diseases[1][2][3][4].

    In Vitro

    Ammonium chloride (for molecular biology) (10 mmol/L) inhibits rapamycin-induced autophagy in human hepatocellular carcinoma HepG2 cells by decreasing phosphorylated SMAD2 levels, and this inhibitory effect is completely reversed by TGFβ1-induced SMAD2 phosphorylation[2].
    Ammonium chloride (2 mM; 24 h) has no significant effect on HeLa human cervical cancer cell viability alone, but enhances cisplatin-induced cell growth inhibition in these cells[3].
    Ammonium chloride (2 mM; 24 h) induces a 4.1% apoptotic rate in HeLa human cervical cancer cells alone, and enhances cisplatin-induced apoptosis to a 19.4% rate in these cells[3].
    Ammonium chloride (2 mM; 24 h) does not induce active caspase-3 expression in HeLa human cervical cancer cells alone, but enhances cisplatin-induced active caspase-3 expression in these cells[3].
    Ammonium chloride (2 mM; 24 h) induces low levels of γ-H2AX expression (DNA double-strand breaks) in HeLa human cervical cancer cells alone, and enhances cisplatin-induced γ-H2AX upregulation (severe DNA double-strand breaks) in these cells[3].
    Ammonium chloride (2 mM; 24 h) increases cleaved caspase-3 levels in HeLa human cervical cancer cells alone, and enhances cisplatin-induced cleaved caspase-3 upregulation in these cells[3].

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

    Ammonium chloride, for molecular biology Related Antibodies

    Cell Viability Assay[3]

    Cell Line: HeLa human cervical cancer cells
    Concentration: 2 mM
    Incubation Time: 24 h
    Result: Had no significant effect on cell viability.
    Enhanced cisplatin-induced cell growth inhibition, resulting in a lower cell viability percentage compared to cisplatin alone.

    Apoptosis Analysis[3]

    Cell Line: HeLa human cervical cancer cells
    Concentration: 2 mM
    Incubation Time: 24 h
    Result: Resulted in an apoptotic rate (sub-G1 peak) of 4.1%.
    Increased the apoptotic rate to 19.4% when combined with cisplatin, compared to 12.5% with cisplatin alone.

    Immunofluorescence[3]

    Cell Line: HeLa human cervical cancer cells
    Concentration: 2 mM
    Incubation Time: 24 h
    Result: Did not induce detectable active caspase-3 expression.
    Increased the intensity of red fluorescence (indicating active caspase-3) compared to cisplatin treatment alone when combined with cisplatin.\nInduced low-intensity green fluorescence (γ-H2AX expression), which was less intense than that induced by cisplatin alone.
    Induced the strongest green fluorescence (γ-H2AX expression) compared to all other treatment groups when combined with cisplatin.

    Western Blot Analysis[3]

    Cell Line: HeLa human cervical cancer cells
    Concentration: 2 mM
    Incubation Time: 24 h
    Result: Increased the ratio of cleaved caspase-3 to β-actin compared to control cells, but to a lesser extent than cisplatin alone.
    Further increased the ratio of cleaved caspase-3 to β-actin compared to cisplatin treatment alone when combined with cisplatin.
    In Vivo

    Ammonium chloride (0.1-10 mM; i.n.; 8 total doses) dose-dependently attenuates ozone-induced airway inflammation, hyperreactivity, and goblet cell hyperplasia in female BALB/c mice by reducing Slc26a4 expression and pro-inflammatory cytokine levels[1].

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

    Animal Model: BALB/c mice with Airway inflammation (6-week-old, female, ozone-induced airway inflammation model)[1]
    Dosage: 0.1 mM; 1 mM; 10 mM
    Administration: i.n.; 8 total doses (5 minutes before ozone exposure on Days 7, 9, 11, 13, 15, 17, 19, and 21)
    Result: Attenuated ozone-induced increases in bronchoalveolar lavage fluid total cells, macrophages, neutrophils, and lymphocytes in a dose-dependent manner.
    Significantly reduced ozone-enhanced lung resistance, goblet cell count, and peribronchial inflammation index to sham-treated levels at 10 mM dose.
    Reduced Slc26a4 protein levels in lung lysates and thiocyanate levels in bronchoalveolar lavage fluid in a dose-dependent manner.
    Reduced ozone-induced Slc26a4 and Muc5ac co-expression in bronchial epithelium at 10 mM dose.
    Markedly downregulated ozone-induced increases in lung lysate levels of IFN-γ, TNF-α, IL-17, mature IL-1β, and p20-activated caspase-1 at 10 mM dose.
    분자량

    53.49

    화학식

    NH4Cl
    CAS No.
    SMILES

    N.Cl
    선적

    Room temperature in continental US; may vary elsewhere.
    보관

    Please store the product under the recommended conditions in the Certificate of Analysis.
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    Ammonium chloride, for molecular biology Related Classifications

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    Keywords:

    Ammonium chloride, for molecular biology12125-02-9Salmiac, for molecular biologyTGF-beta/SmadApoptosisChloride ChannelTransforming growth factor betaCl− ChannelsHeLa human cervical cancer cellsmouse tissuesphosphorylated SMAD2Slc26a4lung tissuesrat primary cortical neuronscancer cellsHepG2 cellsneuroblastoma cellsbronchoalveolar lavage fluidInhibitorinhibitorinhibit

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