Aneurysm

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.

Imidapril hydrochloride (TA-6366) is an orally active dual inhibitor of angiotensin-converting enzyme (ACE) and MMP-9. Imidapril hydrochloride inhibits lipopolysaccharide-induced phosphorylation of c-Jun, MKK4 and JNK in monocytes, and downregulates the production of specific inflammatory factors such as TNF-α and IP-10, thereby exerting anti-inflammatory activity. Imidapril hydrochloride also effectively ameliorates mesangial expansion and reduces urinary albumin excretion by inhibiting angiotensin AngII production, lowering glomerular pressure and oxidative stress, thus delaying disease progression. Imidapril hydrochloride can also directly bind to the active site of MMP-9 to inhibit gelatinase activity, and suppress the enlargement of cerebral aneurysms without altering systemic blood pressure. Imidapril hydrochloride is widely applicable to related studies on autoimmune glomerulonephritis, diabetic nephropathy, cerebral aneurysms and other conditions.

Z6466608628 hydrochloride is a selective PPIL4 molecular glue degrader with human PPIL4 EC₅₀ values of 0.34 µM. Z6466608628 hydrochloride functionally recruits PPIL4 to CRBN, induces CRL4^CRBN-mediated ubiquitylation and degradation of PPIL4. Z6466608628 hydrochloride can be used for the research of intracranial aneurysms^[1].

Z6466608628 is a selective PPIL4 molecular glue degrader with human PPIL4 EC₅₀ values of 0.34 µM. Z6466608628 functionally recruits PPIL4 to CRBN, induces CRL4^CRBN-mediated ubiquitylation and degradation of PPIL4. Z6466608628 can be used for the research of intracranial aneurysms.

Alvelestat tosylate (AZD9668 tosylate) is an orally active, selective inhibitor of neutrophil elastase. Alvelestat tosylate 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 tosylate restores endothelial dysfunction, regulates antioxidant factors, improves the expression of endothelial tight junctions, reduces vascular leakage, and accelerates wound healing. Alvelestat tosylate prevents pulmonary hemorrhage, matrix protein degradation, airspace enlargement, and small airway wall remodeling; and alleviates cigarette-induced inflammatory responses. Alvelestat tosylate inhibits the growth of abdominal aortic aneurysms exacerbated by Porphyromonas gingivalis. Alvelestat tosylate can be used in research related to chronic obstructive pulmonary disease, abdominal aortic aneurysm, radiation-induced skin injury, and bronchiectasis.

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.

Alvelestat-¹³C,d₃ (AZD9668-¹³C,d₃) is the deuterated, ¹³C-labeled Alvelestat (HY-15651). 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.