myocardial toxicity

Bisoprolol, a selective beta-1 adrenergic receptor antagonist, selectively and competitively binds to and blocks beta-1 adrenergic receptors in the heart, thereby with antihypertensive activity and devoid of intrinsic sympathomimetic activity.

D-GsMTx4 TFA, a selective spider venom peptide, is a TRPC1/6 and Piezo2 inhibitor that inhibits cation-permeable mechanosensitive channels (MSCs) belonging to the Piezo and TRP channel families, blocks cation-selective stretch-activated channels (SACs), and attenuates lysophosphatidylcholine (LPC)-induced astrocyte toxicity and microglia reactivity. toxicity and microglia reactivity.D-GsMTx4 TFA prevented myocardial infarction in a mouse model of ischemia/reperfusion and can be used to characterize the role of excitatory MSCs in normal physiology and pathology.

Bisoprolol is a cardioselective β1-adrenergic blocker used for secondary prevention of heart failure, myocardial, angina pectorisinfarction (MI) and mild to moderate hypertension.

1. Coptisine (Coptisin) treatment increases cell viability based on its reversal effect on the enhanced activity of Indoleamine 2, 3-dioxygenase . 2. Coptisine treats myocardial I/R likely through suppressing myocardial apoptosis and inflammation by inhibiting the Rho/ROCK pathway. 3. Coptisine is a potential anti-osteosarcoma drug candidate, via exerting a strong anti-osteosarcoma effect with very low toxicity . 4. Coptisine with a high dosage could inhibit cholesterol synthesis via suppressing the HMGCR expression and promoting the use and excretion of cholesterol via up-regulating LDLR and CYP7A1 expression. 5. Coptisine suppresses adhesion, migration and invasion of MDA-MB-231 breast cancer cells in vitro, the down-regulation of MMP-9 in combination with the increase of TIMP-1 possibly contributing to the anti-metastatic function for breast cancer.

TK-129 is an orally active, potent inhibitor of KDM5B with an IC50 of 44 nM and is low-toxicity. TK-129 exhibits cardioprotective effects by inhibiting KDM5B and blocking the KDM5B-associated Wnt pathway. TK-129 can be used in cardiovascular disease studies to reduce isoprenaline-induced myocardial remodelling and fibrosis in vivo, as well as to reduce ang II-induced activation of cardiac fibroblasts in vitro [1].