Methotrexate disodium

Catalog No.S5097 Batch:S509701

Print

Technical Data

Formula

C20H20N8O5.2Na

Molecular Weight 498.4 CAS No. 7413-34-5
Solubility (25°C)* In vitro Water 99 mg/mL (198.63 mM)
DMSO Insoluble
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description Methotrexate sodium, an analog of folic acid, is a nonspecific inhibitor of the dihydrofolate reductase(DHFR) of bacteria and cancerous cells as well as normal cells. It forms an inactive ternary complex with DHFR and NADPH. Methotrexate (MTX) induces apoptosis.
Targets
hDHFR [4]
(Activated peripheral T cells)
24 nM
In vitro Methotrexate (0.1-10 mM) induces apoptosis of in vitro activated T cells from human peripheral blood. Methotrexate achieves clonal deletion of activated T cells in mixed lymphocyte reactions. Methotrexate can selectively delete activated peripheral blood T cells by a CD95-independent pathway. [1] Methotrexate is taken up by cells via the reduced folate carrier and then is converted within the cells to polyglutamates. Methotrexate leads to diminished production of leukotriene B4 by neutrophils stimulated ex vivo. Methotrexate polyglutamates inhibit the enzyme aminoimidazolecarboxamidoadenosineribonucleotide (AICAR) transformylase more potently than the other enzymes involved in purine biosynthesis. Methotrexate is also known to suppress TNF activity by suppressing TNF-induced nuclear factor-κB activation in vitro, in part related to a reduction in the degradation and inactivation of an inhibitor of this factor, IκBα, and probably related to the release of adenosine. Methotrexate suppresses the production of both TNF and IFN-γ by T-cell-receptor-primed T lymphocytes from both healthy human donors and RA patients. Methotrexate treatment is associated with a significant decrease of TNF-α-positive CD4+ T cells, while the number of T cells expressing the anti-inflammatory cytokine IL-10 increased. [2]
In vivo Methotrexate increases splenocyte AICAR content, raised adenosine concentrations in exudates from carrageenan-inflamed air pouches, and markedly inhibits leukocyte accumulation in inflamed air pouches in mice. Methotrexate-mediated reduction in leukocyte accumulation is partially reversed by injection of adenosine deaminase (ADA) into the air pouch, completely reverses by a specific adenosine A2 receptor antagonist, 3,7-dimethyl-1-propargylxanthine (DMPX), but not affected by an adenosine A1 receptor antagonist, 8-cyclopentyl-dipropylxanthine in mice. [3]

Protocol (from reference)

Selleck's Methotrexate disodium has been cited by 20 publications

Oncogenic β-catenin-driven liver cancer is susceptible to methotrexate-mediated disruption of nucleotide synthesis [ Chin Med J (Engl), 2023, 10.1097/CM9.0000000000002816] PubMed: 37612257
Modulation of Skin Inflammatory Responses by Aluminum Adjuvant [ Pharmaceutics, 2023, 15(2)576] PubMed: 36839900
Multi-omics analysis based on 3D-bioprinted models innovates therapeutic target discovery of osteosarcoma [ Bioact Mater, 2022, 18:459-470] PubMed: 35415297
Metabolic control of CD47 expression through LAT2-mediated amino acid uptake promotes tumor immune evasion [ Nat Commun, 2022, 13(1):6308] PubMed: 36274066
Hydroxychloroquine lowers Alzheimer's disease and related dementias risk and rescues molecular phenotypes related to Alzheimer's disease [ Mol Psychiatry, 2022, none] PubMed: 36577843
Addressing Doxorubicin Resistance in Bone Sarcomas Using Novel Drug-Resistant Models [ Int J Mol Sci, 2022, 23(12)6425] PubMed: 35742867
Lectin galactoside-binding soluble 3 binding protein mediates methotrexate resistance in choriocarcinoma cell lines [ Bioengineered, 2022, 13(2):2076-2086] PubMed: 35038949
A network-based approach to integrate nutrient microenvironment in the prediction of synthetic lethality in cancer metabolism [ PLoS Comput Biol, 2022, 18(3):e1009395] PubMed: 35286311
A study of protein-drug interaction based on solvent-induced protein aggregation by fluorescence correlation spectroscopy [ Analyst, 2022, 10.1039/d2an00031h] PubMed: 35253833
The novel mechanism of Med12-mediated drug resistance in a TGFBR2-independent manner [ Biochem Biophys Res Commun, 2022, 610:1-7] PubMed: 35461070

RETURN POLICY
Selleck Chemical’s Unconditional Return Policy ensures a smooth online shopping experience for our customers. If you are in any way unsatisfied with your purchase, you may return any item(s) within 7 days of receiving it. In the event of product quality issues, either protocol related or product related problems, you may return any item(s) within 365 days from the original purchase date. Please follow the instructions below when returning products.

SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.