| Name | TM5441 |
| Description | TM5441 is an orally bioavailable fibrinogen activator inhibitor-1 inhibitor that inhibits several cancer cell lines with IC50 values ranging from 13.9 to 51.1 μM.It induces intrinsic cell death in several human cancer cells and attenuates Nω-nitro-1-arginine methyl ester-induced cardiac hypertension and vascular senescence. |
| Kinase Assay | TM5441 is dissolved with DMSO at a stock concentration of 50 mM.HT1080, HCT116, Daoy, MDA-MB-231 and Jurkat cells are treated with 0-100 μM TM5441 for 48 hours at 37°C. Cell viability is measured by MTT assay. |
| Animal Research | TM5441 is prepared in 0.5% carboxymethyl cellulose.Mice: TM5275 at 50 mg/kg/day and TM5441 at 10 mg/kg/day were orally administered in control and diabetic mice for 16 weeks. Mice were monitored at least once a day. At the end, blood is collected for measurement of plasma glucose and creatinine, urine for protein measurement, and kidneys for immunohistochemical analysis. |
| In vitro | METHODS: TM5441 (1-100μM) was used to further study the survival of HT1080, HCT116, Daoy, MDA-MB-231 and Jurkat.
RESULTS Cell viability treated with TM5441 significantly decreased in a dose-dependent manner by 50%, ranging between 13.9 and 51.1μM.[2]
METHODS: Cultures of human endothelial cells EA.hy926 were pretreated with TM5441 (10 μM) for 24 h and then treated with doxorubicin (Dox) in triplicate for 4 days. Total protein and RNA were collected from three independently treated wells and combined to explore the protective effect of TM5441 on Dox-induced cellular senescence.
RESULTS TM5441 treatment inhibited Dox-induced expression levels of p53, PAI-1, p16, p21 and IGFBP3 in human endothelial cells. [3] |
| In vivo | METHODS: High-fat diet (HFD)-fed C57BL/6J mice were treated with 20 mg/kg of TM5441 daily to study the effect of TM5441, an oral PAI-1 inhibitor that lacks bleeding risk, on HFD-induced NAFLD.
RESULTS Early and delayed treatment with TM5441 reduced hepatic steatosis, and both strategies abolished hepatic insulin resistance and mitochondrial dysfunction, manifested by enhanced p-Akt and p-GSK3β, reduced p-JNK signaling, and p-AMPK and PGC-1α activation. [1] |
| Storage | Shipping with blue ice/Shipping at ambient temperature. |
| Solubility Information | 10% DMSO+40% PEG300+5% Tween 80+45% Saline : 1 mg/mL (2.33 mM), Sonication is recommended.
DMSO : 5.67 mg/mL (13.22 mM), Sonication is recommended.
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| Keywords | TM-5441 | TM5441 | TM 5441 | Plasminogen activator inhibitor-1 | PAI-1 | PAI1 | Inhibitor | inhibit | Apoptosis |
| Inhibitors Related | Stavudine | Aceglutamide | Urea | Tamoxifen | Cysteamine hydrochloride | Metronidazole | Citric Acid Triammonium | Formamide | Dimethyl phthalate | Alginic acid | Sodium Molybdate | Sildenafil citrate |
| Related Compound Libraries | Apoptosis Compound Library | Target-Focused Phenotypic Screening Library | Bioactive Compound Library | Inhibitor Library | Anti-Cardiovascular Disease Compound Library | NO PAINS Compound Library | Metabolism Compound Library | Orally Active Compound Library | Anti-Aging Compound Library | Bioactive Compounds Library Max | Anti-Cancer Compound Library | Anti-Cancer Active Compound Library |
United States
