cardiac toxicity

Acecainide hydrochloride (NAPA) is a major metabolite of PROCAINAMIDE. Its anti-arrhythmic action may cause cardiac toxicity in kidney failure.

O-Desmethyl Quinidine is a novel quinidine analog with significant antiarrhythmic activity and low acute toxicity that may be useful in the treatment of cardiac arrhythmias.

(R)-Carvedilol is a non-selective blocker of β/α-1. (R)-Carvedilol exerts protection against the vascular or cardiac toxicity of Doxorubicin (DOX).

(S)-Carvedilol is a non-selective β/α-1 blocker.It exerts protection against the vascular or cardiac toxicity of Doxorubicin (DOX).

Levobupivacaine hydrochloride ((S)-(-)-Bupivacaine monohydrochloride) is a reversible neuronal sodium channel inhibitor, which is the pure S(-)-enantiomer of bupivacaine. It was utilized as a long-acting local anesthetic.

Polystyrene microplastics (PS-MPs) are a toxic substance that poses risks to aquatic life, specifically causing cardiac harm to zebrafish and inducing male reproductive toxicity in mice [1] [2].

Fasciculin-I, a toxin isolated from mamba venom, exerts its toxicity primarily by inhibiting acetylcholinesterase (AChE). Additionally, it impedes the action of α-neurotoxins on nicotinic acetylcholine receptors and neutralizes cardiac toxins that interact with cell membranes [1].

(Rac)-Nebivolol ((Rac)-R 065824) is a racemic isomer of Nebivolol. Nebivolol is a selective antagonist of β1-adrenergic receptor (IC 50= 0.8 nM). Nebivolol shows Vasodilatory activity. In the early stages of ethanol-induced cardiac toxicity, Nebivolol can prevent up-regulation of Nox2/NADPH oxidase and lipoperoxidation.

Amrubicin, also known as SM-5887, is an anthracycline used in the treatment of lung cancer. Amrubicin intercalates into DNA and inhibits the activity of topoisomerase II, resulting in inhibition of DNA replication, and RNA and protein synthesis, followed by cell growth inhibition and cell death. This agent has demonstrated a higher level of anti-tumor activity than conventional anthracycline drugs without exhibiting any indication of the cumulative cardiac toxicity common to this class of compounds. It is marketed in Japan since 2002 by Sumitomo Pharmaceuticals.

Antitubercular Agent-38, a derivative of Benzothiazinones (BTZs), demonstrates potent antituberculosis activity while maintaining low cardiac toxicity and minimal cell cytotoxicity [1]. This orally active compound is a promising therapeutic in the treatment of tuberculosis.

Zofenoprilat, an angiotensin-converting enzyme (ACE; IC50 = 8 nM for rabbit lung enzyme) inhibitor and the active metabolite of the prodrug zofenopril, effectively counters angiotensin I- or bradykinin-induced contractions in isolated guinea pig ileum (EC50s = 3 and 1 nM, respectively). At a concentration of 10 nM, Zofenoprilat not only diminishes basal endothelin-1 secretion and nitric oxide (NO) production but also safeguards against TNF-α-stimulated increases in reactive oxygen species (ROS) and reductions in glutathione (GSH) levels within human umbilical vein endothelial cells (HUVECs). Furthermore, at 10 µM, it delivers protection to primary human cardiac microvascular endothelial cells from doxorubicin-induced toxicity and enhances hydrogen sulfide (H2S) production, along with the adhesion, migration, and proliferation of HUVECs. Additionally, Zofenoprilat (400 µM) mitigates end diastolic pressure and lactate dehydrogenase (LDH) release, demonstrating therapeutic potential in a Langendorff isolated perfused rat heart model of ischemia-reperfusion injury.

Levobupivacaine is an amino-amide local anaesthetic drug belonging to the family of n-alkylsubstituted pipecoloxylidide. It is the S-enantiomer of bupivacaine. Levobupivacaine hydrochloride is commonly marketed by AstraZeneca under the trade name Chirocaine. Compared to bupivacaine, levobupivacaine is associated with less vasodilation and has a longer duration of action. It is approximately 13 per cent less potent (by molarity) than racemic bupivacaine.Levobupivacaine is indicated for local anaesthesia including infiltration, nerve block, ophthalmic, epidural and intrathecal anaesthesia in adults; and infiltration analgesia in children. Adverse drug reactions (ADRs) are rare when it is administered correctly. Most ADRs relate to administration technique (resulting in systemic exposure) or pharmacological effects of anesthesia, however allergic reactions can rarely occur.

TK-129 is an orally active, potent inhibitor of KDM5B with IC 50 of 44 nM that is low-toxicity. TK-129 shows cardioprotective effects by inhibiting KDM5B and blocking the KDM5B -associated Wnt pathway. TK-129 can be used in cardiovascular disease studies which reduce isoprenaline-induced myocardial remodelling and fibrosis in vivo as well as reduce ang II-induced activation of cardiac fibroblasts in vitro [1].

Uridine triacetate (RG 2133 triacetate) (Tri-O-acetyl uridine), an orally active prodrug of uridine, is efficiently absorbed in the gut and swiftly deacetylated in the circulation to release free uridine. It is utilized in the research of 5-fluorouracil (5-FU) and capecitabine toxicity, particularly targeting early-onset cardiac or central nervous system (CNS) complications.