Sulfasalazine

Catalog No.S1576 Batch:S157604

Print

Technical Data

Formula

C18H14N4O5S

Molecular Weight 398.39 CAS No. 599-79-1
Solubility (25°C)* In vitro DMSO 80 mg/mL (200.8 mM)
Water Insoluble
Ethanol 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 Sulfasalazine is a sulfa derivative of mesalazine, used as an anti-inflammatory agent to treat bowel disease and rheumatoid arthritis. Sulfasalazine is a potent and specific inhibitor of nuclear factor kappa B (NF-κB), TGF-β and COX-2. Sulfasalazine induces ferroptosis, apoptosis and autophagy.
Targets
NF-κB [4] COX-2 [4] TGF-β [4]
In vitro

Sulfasalazine, like methotrexate, enhances adenosine release at an inflamed site and that adenosine diminishes inflammation via occupancy of A2 receptors on inflammatory cells. [1] Sulfasalazine treatment for 4 hours inhibits kappaB-dependent transcription with an IC50 value of approximately 0.625 mM. Sulfasalazine (2.5 mM) results in cell death of T-lymphocytes in a dose- and time-dependent manner. Sulfasalazine but not 5ASA or sulfapyridine, strongly inhibits NF-kappaB activation and potently induces apoptosis in T-lymphocytes. [2] Sulfasalazine is cleaved into sulfapyridine and 5-aminosalicylic acid (5-ASA; mesalamine) by colonic bacteria, and the latter, too, is reported to suppress NF-kappaB activity. Sulfasalazine but not its cleaved form 5-ASA causes a dose-dependent inhibition of glioma growth, this effect is entirely attributable to the inhibition of cystine uptake via the system x(c)(-) cystine-glutamate transporter. Sulfasalazine inhibits cystine uptake causing a chronic depletion of intracellular GSH and consequently compromised cellular redox defense which stymied tumor growth. [3]

In vivo

Sulfasalazine markedly decreases the number of leukocytes that accumulated in the inflamed (carrageenan, 2 mg/ml) air pouch in the murine air pouch model of inflammation. Sulfasalazine treatment promotes a marked increase in splenocyte 5-aminoimidazole-4-carboxamidoribonucleotide (AICAR) concentration, which is consistent with the in vitro observation that sulfasalazine inhibits AICAR transformylase. [1]

Protocol (from reference)

Selleck's Sulfasalazine has been cited by 17 publications

Ferroptosis-Enhanced Immunotherapy with an Injectable Dextran-Chitosan Hydrogel for the Treatment of Malignant Ascites in Hepatocellular Carcinoma [ Adv Sci (Weinh), 2023, 10(20):e2300517] PubMed: 37132587
Mitochondrial outer membrane protein FUNDC2 promotes ferroptosis and contributes to doxorubicin-induced cardiomyopathy [ Proc Natl Acad Sci U S A, 2022, 119(36):e2117396119] PubMed: 36037337
AUF1 protects against ferroptosis to alleviate sepsis-induced acute lung injury by regulating NRF2 and ATF3 [ Cell Mol Life Sci, 2022, 79(5):228] PubMed: 35391558
Intratarget Microdosing for Deep Phenotyping of Multiple Drug Effects in the Live Brain [ Front Bioeng Biotechnol, 2022, 10:855755] PubMed: 35372313
High-throughput in situ perturbation of metabolite levels in the tumor micro-environment reveals favorable metabolic condition for increased fitness of infiltrated T-cells [ Front Cell Dev Biol, 2022, 10:1032360] PubMed: 36619865
Peroxidation of n-3 and n-6 polyunsaturated fatty acids in the acidic tumor environment leads to ferroptosis-mediated anticancer effects [ Cell Metab, 2021, S1550-4131(21)00233-3] PubMed: 34118189
DCN released from ferroptotic cells ignites AGER-dependent immune responses [ Autophagy, 2021, 10.1080/15548627.2021.2008692] PubMed: 34964698
PARP inhibition promotes ferroptosis via repressing SLC7A11 and synergizes with ferroptosis inducers in BRCA-proficient ovarian cancer [ Redox Biol, 2021, S2213-2317(21)00076-8] PubMed: 33722571
STING1 Promotes Ferroptosis Through MFN1/2-Dependent Mitochondrial Fusion [ Front Cell Dev Biol, 2021, 9:698679] PubMed: 34195205
SMG9 drives ferroptosis by directly inhibiting GPX4 degradation [ Biochem Biophys Res Commun, 2021, 567:92-98] PubMed: 34146907

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.