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Su5416

Manufactured by Targetmol
Sourced in United States

SU5416 is a small-molecule inhibitor that targets the vascular endothelial growth factor receptor (VEGFR) tyrosine kinase. It is used in research applications to study angiogenesis and related cellular processes.

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2 protocols using su5416

1

Evaluation of Small Molecule Compounds

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SU5416(CAS 204005–46-9) and Cell Counting Kit-8 (CCK-8) (CAS C0005) purchased from TargetMol, Trimetazidine (TMZ) was obtained from Servier (Tianjin). 3-TYP (S8628) was purchased from selleck.cn. β-Sitosterol (CAS 83–46–5), luteolin (CAS 491–70–3), Kaempferol (CAS 520–18–3), Costunolide (CAS 553–21–9), Naringenin (CAS 480–41–1),and Quercetin (CAS 117–39–5)were purchased from Chengdu Ruifensi Biotechnology Co., Ltd. (Sichuan, P. R. China).
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2

Hypoxia-induced Pulmonary Hypertension in miRNA-30a Knockout Mice

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miRNA-30a KO mice were obtained under license from Nanjing Biomedical Research Institute of Nanjing University (project no. XM001304). miR-30a KO mice or age-matched WT controls (strain C57BL/6, 8 weeks of age) were randomly divided into 4 groups: (1) a vehicle-normoxia-treated WT group (WT+Nor/Veh) (n = 10); (2) a Su5416-hypoxia-treated WT group (WT+Su/Hx) (n = 10); (3) a vehicle-normoxia-treated miR-30a−/− group (miR-30a KO+Nor/Veh) (n = 6); and (4) a Su5416-hypoxia-treated miRNA-30a−/− group (miR-30a KO+Su/Hx) (n = 8). The WT+Su/Hx and miR-30a KO+Su/Hx groups were injected subcutaneously with Su5416 (20 mg/kg, TargetMol, Boston, MA, USA) weekly, which was suspended in CMC (0.5% [w/v] carboxymethylcellulose sodium, 0.9% [w/v] sodium chloride, 0.4% [v/v] polysorbate 80, 0.9% [v/v] benzyl alcohol in deionized water) as previously described.42 (link) Then, the animals were exposed to chronic normobaric hypoxia (10% O2) in a chamber for 21 days. The WT+Nor/Veh and miR-30a KO+Nor/Veh groups received only vehicle, and then the animals were kept in room air. At study termination, mice were anesthetized and sacrificed. A schematic of the experimental design is illustrated in Figure S1A.
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