1209 Results for "

synthases

" in MedChemExpress (MCE) Product Catalog:
Products (1209)

1209 Results for "synthases" in MCE Product Catalog:

Cat. No.: HY-L044
593 compounds

Nucleoside and nucleotide analogues are synthetic, chemically modified compounds that have been developed to mimic their physiological counterparts in order to exploit cellular metabolism and subsequently be incorporated into DNA and RNA to inhibit cellular division and viral replication. In addition to their incorporation into nucleic acids, nucleoside and nucleotide analogues can interact with and inhibit essential enzymes such as human and viral polymerases (that is, DNA-dependent DNA polymerases, RNA-dependent DNA polymerases or RNA-dependent RNA polymerases), kinases, ribonucleotide reductase, DNA methyltransferases, purine and pyrimidine nucleoside phosphorylase and thymidylate synthase. These actions of nucleoside and nucleotide analogues have potential therapeutic benefits — for example, in the inhibition of cancer cell growth, the inhibition of viral replication as well as other indications.

MCE offers a unique collection of 593 nucleotide compounds including nucleotide, nucleoside and their structural analogues. MCE Nucleotide Compound Library is a useful tool to discover anti-cancer and antiviral drugs for high throughput screening (HTS) and high content screening (HCS).

Cat. No.: HY-100977S
CAS No.: 3006902-95-7
Synonyms: DiMC-d6; CHC 004-d6; Di-O-methylcurcumin-d6
Dimethoxycurcumin-d6 (DiMC-d6; CHC 004-d6; Di-O-methylcurcumin-d6) is the deuterated-labeled Dimethoxycurcumin (HY-100977). Dimethoxycurcumin (DiMC) is a curcuminoid compound found in Curcuma longa. Dimethoxycurcumin is also an orally active thioredoxin reductase inhibitor (IC50 = 5.4 μM) and androgen receptor antagonist. Dimethoxycurcumin inhibits thioredoxin reductase, leading to oxidized thioredoxin accumulation, ROS production, DNA damage, glutathione depletion, mitochondrial membrane potential decrease, ATP depletion, S phase arrest, and apoptosis. Dimethoxycurcumin inhibits NF-κB, NADPH oxidase subunits, ATP synthase subunits, CDK4, cyclin-D1, FASN, ACC, and the IRS2-PI3K-Akt pathway, while activating AMPK, ERK, and JNK. Dimethoxycurcumin can be used for research on cancer, arsenic-induced hepatotoxicity, and tuberculosis .
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Cat. No.: HY-128866
CAS No.: 2332841-25-3
Target:  

Bacterial

Research Areas:  

Infection

TBAJ-876 is an orally active diarylquinoline anti-Mycobacterium agent. TBAJ-876 regulates energy metabolism by targeting the c and ε subunits of Mycobacterium tuberculosis F-ATP synthase, exerts bactericidal activity against replicating Mycobacterium tuberculosis, and retains activity against strains carrying the Rv0678 mutation. TBAJ-876 undergoes N-demethylation in vivo to form its major active metabolite TBAJ-876-M3, which has lower lipophilicity and hERG potassium channel binding affinity. TBAJ-876 is well tolerated in BALB/c mice and significantly reduces the colony-forming units of Mycobacterium tuberculosis in the lungs. In addition, TBAJ-876 exhibits inhibitory activity against Mycobacterium abscessus, reduces bacterial loads in the lungs and spleens of infected mice, and shows no antagonistic effect when used in combination with common antibiotics. TBAJ-876 can be used in studies related to tuberculosis and Mycobacterium abscessus pulmonary diseases .
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Cat. No.: HY-134160S
CAS No.: 1189492-99-6
Synonyms: 5-DHFU-13C,15N2; 5-Fluorodihydropyrimidine-2,4-dione-13C,15N2; 5-Fluorodihydrouracil-13C,15N2
5,6-Dihydro-5-Fluorouracil- 13C, 15N2 (5-DHFU- 13C, 15N2) is the 13C- and 15N-labeled labeled 5,6-Dihydro-5-Fluorouracil (HY-134160). 5,6-Dihydro-5-Fluorouracil (5-DHFU; 5-Fluorodihydropyrimidine-2,4-dione) is the active metabolite of the thymidylate synthase inhibitor prodrug 5-fluorouracil (HY-90006), which is formed from 5-fluorouracil by dihydropyrimidine dehydrogenase (DPD). 5,6-Dihydro-5-Fluorouracil is cytotoxic to HaCaT keratinocytes (IC50=13.5 μM). Intravenous administration of 5,6-Dihydro-5-Fluorouracil (90 mg/kg/wk) in combination with 5-fluorouracil and the DPD inhibitor eniluracil (HY-10533) slows tumor growth in a rat colon cancer model.
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Cat. No.: HY-165587
CAS No.: 284464-83-1
Research Areas:  

Cardiovascular Disease

BM-573 is an orally active dual thromboxane A₂ (TXA₂) modulator with an IC50 of 1.3 nM. BM-573 possesses both thromboxane synthase (TxAS) inhibition and thromboxane receptor (TP) antagonistic effects. BM-573 can completely inhibit platelet aggregation induced by Arachidonic acid (HY-109590) or U-46619 (TXA₂ analogues). BM-573 completely blocks the generation of TXB₂ (the stable metabolite of TXA₂) in human platelets and does not inhibit cyclooxygenase (COX-1/COX-2), thus avoiding interference with other prostaglandin synthesis. BM-573 has an inhibitory effect on U-46619-induced contractions in rat gastric fundus smooth muscle (ED₅₀ = 4.2 μM), but has no effect on contractions caused by PGE₂, PGF₂α, or PGI₂. BM-573 can be used in the study of atherosclerosis, myocardial infarction, pulmonary hypertension and shock .
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Cat. No.: HY-183483
CAS No.: 75987-18-7
Research Areas:  

Cardiovascular Disease

OKY-1581 is a potent, orally active and selective thromboxane A2 synthase inhibitor. OKY-1581 inhibits TXA2 synthesis and reduces the generation of its stable metabolite TXB2. OKY-1581 shifts arachidonic acid (MCE HY-109590) metabolism toward the production of prostaglandin E, prostaglandin F and 6-keto-prostaglandin F1α. OKY-1581 modulates the TXA2 / PGI2-related eicosanoid balance and inhibits arachidonic acid-induced platelet aggregation without directly inhibiting the cyclooxygenase step. At high oral doses, OKY-1581 also enhances hepatic peroxisomal β-oxidation and reduces serum triglyceride and cholesterol levels. OKY-1581 attenuates cerebral vasospasm after experimental subarachnoid hemorrhage by reducing TXA2-related vasoconstrictive signaling. OKY-1581 can be used in studies of atherosclerosis, cerebral vasospasm after subarachnoid hemorrhage and cardiovascular diseases .
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Cat. No.: HY-W778236
CAS No.: 1346603-47-1
Synonyms: SAN 9789-13C,d3
Norflurazon- 13C,d3 (SAN 9789- 13C,d3) is the d3, 13C-labeled Norflurazon (HY-114849). Norflurazon (SAN 9789) is a pre-emergence Herbicide. Norflurazon non-competitively inhibits phytoene desaturase by competing with the enzyme cofactor and disrupts carotenoid biosynthesis, thereby leading to chlorophyll photodegradation and chlorosis. Norflurazon inhibits MGDG synthase, CDP-choline phosphotransferase, Omega-3 FAD7 desaturase, and PG delta-3-trans desaturase, and activates LysoPC-acyltransferase and Omega-3 FAD3 desaturase. Norflurazon inhibits photosynthetic membrane organization, mitochondrial respiration, ATP production, PI3K signaling, and ERK1/2 phosphorylation. Norflurazon activates MAPK P38 phosphorylation and ER stress signaling. Norflurazon induces morphological malformations and cardiovascular effects in zebrafish embryos .
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Cat. No.: HY-125740R
CAS No.: 7228-78-6
Synonyms: Malvidin-3-O-glucoside chloride (Standard); Oenin chloride (Standard)
Malvidin-3-glucoside (Malvidin-3-O-glucoside; Oenin) chloride (Standard) is the analytical standard of Malvidin-3-glucoside chloride (HY-125740). This product is intended for research and analytical applications. Malvidin-3-glucoside chloride is an orally active inhibitor of the NF-κB pathway, which blocks inflammatory responses induced by TNF-α, reduces IκB-α degradation and p65 nuclear translocation, and upregulates endothelial nitric oxide synthase eNOS to increase NO production. Malvidin-3-glucoside chloride exerts anti-inflammatory and antioxidant effects by inhibiting pro-inflammatory molecules such as MCP-1, ICAM-1, and IL-6, and regulating intestinal microorganisms and metabolites, while protecting endothelial cells and improving intestinal microecological dysbiosis under inflammatory conditions. Malvidin-3-glucoside chloride can be used to study chronic inflammatory-related diseases such as atherosclerosis and inflammatory bowel disease, and has the potential to prevent vascular inflammation and improve intestinal health .
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Cat. No.: HY-W127487
CAS No.: 479050-96-9
Quorum sensing is a regulatory system used by bacteria to control gene expression in response to increased cell density. This regulatory process manifests itself in a variety of phenotypes, including biofilm formation and virulence factor production. Coordinated gene expression is achieved through the production, release and detection of small diffusible signaling molecules called autoinducers. N-acylated homoserine lactones (AHLs) comprise a class of such autoinducers, each of which generally consists of a fatty acid coupled to a homoserine lactone (HSL). Modulation of bacterial quorum-sensing signaling systems to suppress pathogenesis represents a new approach to antimicrobial research for infectious diseases. AHLs differ in acyl length (C4-C18), C3 substitution (hydrogen, hydroxyl, or oxo group), and the presence or absence of one or more carbon-carbon double bonds in the fatty acid chain. These differences confer signaling specificity through the affinity of the LuxR family of transcriptional regulators. C18-HSL, one of four lipophilic long acyl side chain AHLs produced by the LuxI AHL synthase homolog SinI, is involved in quorum-sensing signaling in strains of Rhizobium meliloti (a nitrogen-fixing bacterial symbiont of the legume M. sativa) . C18-HSL and other hydrophobic AHLs tend to localize in the relatively lipophilic environment of bacterial cells and cannot diffuse freely across the cell membrane. Long-chain N-acyl homoserine lactones can be exported from cells by efflux pumps, or can be transported between communicating cells by extracellular outer membrane vesicles.
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