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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
521 Results for "
pollen wall
" in MedChemExpress (MCE) Product Catalog:
Products (521)
521 Results for "pollen wall" in MCE Product Catalog:
Cat. No.: HY-N0378S
Synonyms: Mannitol-d8; Mannite-d8
Cat. No.: HY-N0378S1
CAS No.: 132202-29-0
Synonyms: Mannitol-13C; Mannite-13C
Cat. No.: HY-N0378S2
CAS No.: 287112-34-9
Synonyms: Mannitol-13C6; Mannite-13C6
Cat. No.: HY-N0378S4
CAS No.: 2649096-16-0
Synonyms: Mannitol-d2; Mannite-d2
Cat. No.: HY-N0378S5
CAS No.: 75607-68-0
Synonyms: Mannitol-d1; Mannite-d1
Cat. No.: HY-L914
3,211 compounds
In the research of covalent inhibitors targeting serine and threonine, scientists have found that the nucleophilicity of these hydroxyl groups is significantly enhanced due to the influence of their surrounding environment. This results in higher activity during catalytic reactions. Aspirin, which targets the non-catalytic domain serine (Ser529 in human COX1) of cyclooxygenase, exerts its anti-inflammatory effect through covalent binding. β-lactam antibiotics, which targets the catalytic domain serine of penicillin-binding proteins, interferes with bacterial cell wall synthesis.
Through careful selection, we constructed a structural filter containing over 110 electrophilic groups. By analyzing the electrophilic fragments selected by the structural filter, we removed any molecules with trivial or undesirable structural features. Ultimately, we obtained 3,300 fragment molecules which can target serine and threonine residues and can be used for fragment-based covalent drug discovery.
Cat. No.: HY-178413S
Synonyms: Mannitol-d4; Mannite-d4
Cat. No.: HY-183393
CAS No.: 1798292-13-3
NVP-BHS345 is an ATP-competitive TORC1/TORC2 inhibitor with an IC50 of 1 μM for both targets in yeast. NVP-BHS345 acutely inhibits TORC1/TORC2 kinase activity, even in genetically engineered TOR1 M2282T Saccharomyces cerevisiae strains. NVP-BHS345 also reduces the phosphorylation levels of Ser-232/Ser-233 sites in Sch9, Ypk1/Ypk2 and Rps6, and induces hyperphosphorylation of Slt2 and activation of the cell wall integrity pathway. NVP-BHS345 causes depolarization of the actin cytoskeleton, blocks fluid-phase endocytosis, prevents the accumulation of vacuolar lipophilic dyes, and regulates the phosphorylation levels of Ent1, Pan1, Prk1, Akl1 and other cellular proteins .
Cat. No.: HY-N0378S3
CAS No.: 287100-69-0
Synonyms: Mannitol-2-13C; Mannite-2-13C
Cat. No.: HY-N0378S6
CAS No.: 1217463-58-5
Synonyms: Mannitol-13C,d2; Mannite-13C,d2
Cat. No.: HY-N7101S
Synonyms: U-76-d7,252-d7; CS-807-d7
Cat. No.: HY-W015551
CAS No.: 3913-81-3
Synonyms: (E)-Dec-2-enal
Cat. No.: HY-L048
585 compounds
The high rates of morbidity and mortality caused by fungal infections are associated with the current limited antifungal arsenal and the high toxicity of the compounds. Additionally, identifying novel drug targets is challenging because there are many similarities between fungal and human cells. The most common antifungal targets include fungal RNA synthesis and cell wall and membrane components, though new antifungal targets are being investigated. Nonetheless, fungi have developed resistance mechanisms, such as overexpression of efflux pump proteins, overexpression and changes in drug targets and biofilm formation, emphasizing the importance of discovering new antifungal drugs and therapies. Due to the limited antifungal arsenal, researchers have sought to improve treatment via different approaches, such as the combination of antifungal drugs, development of new formulations for antifungal agents and modifications to the chemical structures of traditional antifungals, etc.
MCE offers a unique collection of 585 compounds with validated antifungal activities. MCE antifungal compound library is an effective tool for drug repurposing screening, combination screening and biological investigation.
Cat. No.: HY-15651R
CAS No.: 848141-11-7
Synonyms: AZD9668 (Standard)
Research Areas:
Cardiovascular Disease Neurological Disease Inflammation/Immunology
Alvelestat (Standard) (AZD9668 (Standard)) is the analytical standard of Alvelestat (HY-15651). This product is intended for research and analytical applications. Alvelestat (AZD9668) is an orally active, selective inhibitor of neutrophil elastase. Alvelestat reduces elastase activity, myeloperoxidase release, neutrophil recruitment and activation, and calcium phosphate precipitation; promotes smooth muscle cell colonization and collagen deposition; and inhibits the formation of neutrophil extracellular traps (NETs) as well as NET-derived neutrophil elastase activity. Alvelestat restores endothelial dysfunction, regulates antioxidant factors, improves the expression of endothelial tight junctions, reduces vascular leakage, and accelerates wound healing. Alvelestat prevents pulmonary hemorrhage, matrix protein degradation, airspace enlargement, and small airway wall remodeling; and alleviates cigarette-induced inflammatory responses. Alvelestat inhibits the growth of abdominal aortic aneurysms exacerbated by Porphyromonas gingivalis. Alvelestat can be used in research related to chronic obstructive pulmonary disease, abdominal aortic aneurysm, radiation-induced skin injury, and bronchiectasis .
Cat. No.: HY-15651S
Synonyms: AZD9668-13C,d3
Cat. No.: HY-W015551R
CAS No.: 3913-81-3
Synonyms: (E)-Dec-2-enal (Standard)
Cat. No.: HY-W015551S
CAS No.: 1335436-39-9
Synonyms: (E)-Dec-2-enal-d2
Cat. No.: HY-P992076
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
