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Results for "

cardiac toxicity

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Adrenergic Receptor (5) Apoptosis (2) Autophagy (1) Bacterial (1) Cholinesterase (ChE) (1) Ferroptosis (2) Fluorescent Dye (2) Histone Demethylase (1) Isotope-Labeled Compounds (3) NADPH Oxidase (1) Sodium Channel (2) TGF-β Receptor (1) Toll-like Receptor (TLR) (1)
By Research Areas:	Cancer (3) Cardiovascular Disease (6) Infection (1) Inflammation/Immunology (2) Neurological Disease (4)

Inhibitors & Agonists

Screening Libraries

Fluorescent Dye

Peptides

Natural
Products

Isotope-Labeled Compounds

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-B0006B

(S)-Carvedilol (S)-BM 14190	Adrenergic Receptor	Cardiovascular Disease
(S)-Carvedilol, the S-enantiomer of Carvedilol, is a non-selective β/α-1 blocker. (S)-Carvedilol exerts protection against the vascular or cardiac toxicity of Doxorubicin (DOX) .

HY-B0006C

(R)-Carvedilol (R)-BM 14190	Adrenergic Receptor	Cardiovascular Disease
(R)-Carvedilol ((R)-BM 14190), the R-enantiomer of Carvedilol, is a non-selective β/α-1 blocker. (R)-Carvedilol exerts protection against the vascular or cardiac toxicity of Doxorubicin (DOX) .

HY-B0653A

Levobupivacaine hydrochloride 2 Publications Verification (S)-(-)-Bupivacaine monohydrochloride	Sodium Channel Ferroptosis	Neurological Disease Cancer
Levobupivacaine hydrochloride ((S)-(-)-Bupivacaine monohydrochloride) is a long-acting amide local anaesthetic. Levobupivacaine hydrochloride exerts anaesthetic and analgesic effects through reversible blockade of neuronal sodium channel. Levobupivacaine hydrochloride can inhibit impulse transmission and conduction in cardiovascular and other tissues, possessing certain cardiac and CNS toxicity. Levobupivacaine hydrochloride is metabolized by hepatic cytochrome P450 (CYP450) enzymes in vivo. Levobupivacaine hydrochloride can also induce ferroptosis by miR-489-3p/SLC7A11 signaling in gastric cancer .

HY-B0203B

(Rac)-Nebivolol (Rac)-R 065824	Adrenergic Receptor NADPH Oxidase	Cardiovascular Disease
(Rac)-Nebivolol ((Rac)-R 065824) is a racemic isomer of Nebivolol. Nebivolol is a selective β1-adrenergic receptor antagonist with an IC₅₀ value of 0.8 nM. Nebivolol can prevent up-regulation of Nox2/NADPH oxidase and lipoperoxidation in the early stages of ethanol-induced cardiac toxicity. Vasodilatory activity .

HY-B0653

Levobupivacaine (S)-(-)-Bupivacaine	Sodium Channel Ferroptosis	Neurological Disease Cancer
Levobupivacaine ((S)-(-)-Bupivacaine) is a long-acting amide local anaesthetic. Levobupivacaine exerts anaesthetic and analgesic effects through reversible blockade of neuronal sodium channel. Levobupivacaine can inhibit impulse transmission and conduction in cardiovascular and other tissues, possessing certain cardiac and CNS toxicity. Levobupivacaine is metabolized by hepatic cytochrome P450 (CYP450) enzymes in vivo. Levobupivacaine can also induce ferroptosis by miR-489-3p/SLC7A11 signaling in gastric cancer .

HY-D0711

Indocyanine green Maximum Cited Publications 18 Publications Verification Foxgreen; IC Green; Cardiogreen	Fluorescent Dye	Others
Indocyanine green (Foxgreen) is a low toxicic fluorescent agent that has been widely used in medical diagnostics, such as determining cardiac output, hepatic function, and liver blood flow, and for ophthalmic angiography .

HY-155067

Antitubercular agent-38	Bacterial	Infection
Antitubercular agent-38 is an orally active Benzothiazinones (BTZs) derivate, with potent antituberculosis activity. Antitubercular agent-38 exhibits low cardiac toxicity, low cell cytotoxicity .

HY-P5798

Fasciculin-I FAS-I	Cholinesterase (ChE)	Neurological Disease
Fasciculin-I is isolated from the mambas venom. Fasciculin-I exerts its toxic effects by inhibiting acetylcholinesterase (AChE). Fasciculin-I blocks α-neurotoxins of nicotinic acetylcholine receptors and cardiac toxins that interact with cell membranes .

HY-N6664

Gum arabic Arabic gum	Others	Others
Gum Arabic (Arabic gum) is a branched-chain, complex polysaccharide derive from A. Senegal. Gum Arabic is an anti-oxidant, and can protect against experimental hepatic-, renal- and cardiac toxicities. Gum Arabic also can be used in immunohistochemistry .

HY-B0006BS

(S)-Carvedilol-d4 (S)-BM 14190-d₄	Isotope-Labeled Compounds Adrenergic Receptor	Cardiovascular Disease
(S)-Carvedilol-d₄ is deuterium labeled (S)-Carvedilol. (S)-Carvedilol, the S-enantiomer of Carvedilol, is a non-selective β/α-1 blocker. (S)-Carvedilol exerts protection against the vascular or cardiac toxicity of Doxorubicin (DOX)[1].

HY-B0006CS

(R)-Carvedilol-d4 (R)-BM 14190-d₄	Isotope-Labeled Compounds Adrenergic Receptor	Cardiovascular Disease
(R)-Carvedilol-d₄ is deuterium labeled (R)-Carvedilol. (R)-Carvedilol ((R)-BM 14190), the R-enantiomer of Carvedilol, is a non-selective β/α-1 blocker. (R)-Carvedilol exerts protection against the vascular or cardiac toxicity of Doxorubicin (DOX)[1].

HY-125851

TP-008	TGF-β Receptor	Inflammation/Immunology
TP-008 is a potent, selective and orally active (Activin-Like Kinase 5) ALK5 inhibitor with pIC₅₀ and pEC₅₀ values of 7.6 and 6.63, respectively. TGFβRI-IN-2 can produce observed cardiac toxicity in vivo at high dose .

HY-D0711S2

Indocyanine green-d7 Foxgreen-d₇; IC Green-d₇; Cardiogreen-d₇	Isotope-Labeled Compounds Fluorescent Dye	Others
Indocyanine green-d7 (Foxgreen-d7) is the deuterium labeled Indocyanine green (HY-D0711). Indocyanine green is a low toxicic fluorescent agent that has been widely used in medical diagnostics, such as determining cardiac output, hepatic function, and liver blood flow, and for ophthalmic angiography .

HY-14905

Uridine triacetate Tri-O-acetyl uridine	Others	Neurological Disease
Uridine triacetate (Tri-O-acetyl uridine) is an orally active proagent of Uridine (HY-B1449). Uridine triacetate is quickly absorbed in the gut, and is rapidly deacetylated in the circulation to yield free uridine. Uridine triacetate is used for the research of 5-fluorouracil (5-FU) and capecitabine toxicity, or early-onset cardiac or central nervous system (CNS) .

HY-N1346

Robinin 1 Publications Verification	Toll-like Receptor (TLR) Apoptosis	Inflammation/Immunology
Robinin is a flavonoid that can be extracted from the leaves of purple cowpea, inhibiting TGF-β, TLR4/NF-κB and TLR2-PI3k-AKT signaling pathways. Robinin exerts anti-inflammatory and anti-tumor effects. The combination of Robinin and Methotrexate (HY-14519) reduces inflammation in experimental arthritis, Robinin can decrease the Doxorubicin (HY-15142A) induced cardiac toxicity effect .

HY-151483

TK-129	Histone Demethylase	Cardiovascular Disease
TK-129 is an orally active, low-toxicity, potent KDM5B inhibitor (with high affinity; IC₅₀=44 nM). TK-129 exerts cardioprotective effects by inhibiting KDM5B and blocking the KDM5B-associated Wnt pathway. TK-129 reduces ang II-induced activation of cardiac fibroblasts in vitro and reduces isoprenaline-induced myocardial remodelling and fibrosis in vivo. TK-129 can be used in studies of cardiovascular disease .

HY-N0124

Dioscin 5+ Cited Publications Collettiside III; CCRIS 4123	Autophagy Apoptosis	Cancer
Dioscin (CCRIS 4123; Collettiside III) is a natural plant-derived steroidal saponin that has good anti-cancer activity against a variety of cancer cells. Dioscin causes DNA damage and induces apoptosis in HeLa and SiHa cells. Dioscin regulates ROS-mediated DNA damage and mitochondrial signaling pathways, exerting anticancer activity .

Cat. No.	Product Name

HY-L076

Drug-Induced Liver Injury (DILI) Compound Library	1391 compounds
Drug-induced liver injury (DILI; also known as drug-induced hepatotoxicity) is caused by medications (prescription or OTC), herbal and dietary supplements (HDS), or other xenobiotics that result in abnormalities in liver tests or in hepatic dysfunction that cannot be explained by other causes. Drugs are an important cause of liver injury. Drug-induced hepatic injury is the most common reason cited for withdrawal of an approved drug. DILI is thought to occur via several different mechanisms. Among these are direct impairment of the structural (e.g., mitochondrial dysfunction) and functional integrity of the liver; production of a metabolite that alters hepatocellular structure and function; production of a reactive drug metabolite that binds to hepatic proteins to produce new antigenic drug-protein adducts, which are targeted by hosts’ defenses (the hapten hypothesis); and initiation of a systemic hypersensitivity response (i.e., drug allergy) that damages the liver. MCE Drug-induced Liver Injury (DILI) Compound Library contains a unique collection of 1391 hepatotoxicity causing compounds and is a powerful tool to research DILI and other drug toxicities. This library can be used to understand the mechanisms of DILI, identify biomarkers for early DILI prediction, and allow timely recognition during drug development, thus finally achieving successful DILI prevention and assessment in the pre-marketing phase.

Drug-Induced Liver Injury (DILI) Compound Library

1391 compounds

Drug-induced liver injury (DILI; also known as drug-induced hepatotoxicity) is caused by medications (prescription or OTC), herbal and dietary supplements (HDS), or other xenobiotics that result in abnormalities in liver tests or in hepatic dysfunction that cannot be explained by other causes. Drugs are an important cause of liver injury. Drug-induced hepatic injury is the most common reason cited for withdrawal of an approved drug.

DILI is thought to occur via several different mechanisms. Among these are direct impairment of the structural (e.g., mitochondrial dysfunction) and functional integrity of the liver; production of a metabolite that alters hepatocellular structure and function; production of a reactive drug metabolite that binds to hepatic proteins to produce new antigenic drug-protein adducts, which are targeted by hosts’ defenses (the hapten hypothesis); and initiation of a systemic hypersensitivity response (i.e., drug allergy) that damages the liver.

MCE Drug-induced Liver Injury (DILI) Compound Library contains a unique collection of 1391 hepatotoxicity causing compounds and is a powerful tool to research DILI and other drug toxicities. This library can be used to understand the mechanisms of DILI, identify biomarkers for early DILI prediction, and allow timely recognition during drug development, thus finally achieving successful DILI prevention and assessment in the pre-marketing phase.

HY-L155

Mitochondrial Toxicity Compound Library	470 compounds
Mitochondria, as the main place of energy supply in life, is essential to maintain normal life activities. Mitochondrial dysfunction is associated with common diseases, such as cardiovascular diseases, neurodegenerative diseases, diabetes and cancer. The heart, brain and liver rely heavily on mitochondrial function as the main organs for drug metabolism. In addition, mitochondria is also a target of many drugs, some of which induce organotoxicity by inducing mitochondrial toxicity. MCE contains 470 mitochondrial toxic compounds, which can be used as tool compounds for drug development, organ toxicity and disease mechanism research.

Mitochondrial Toxicity Compound Library

470 compounds

Mitochondria, as the main place of energy supply in life, is essential to maintain normal life activities. Mitochondrial dysfunction is associated with common diseases, such as cardiovascular diseases, neurodegenerative diseases, diabetes and cancer. The heart, brain and liver rely heavily on mitochondrial function as the main organs for drug metabolism. In addition, mitochondria is also a target of many drugs, some of which induce organotoxicity by inducing mitochondrial toxicity.

MCE contains 470 mitochondrial toxic compounds, which can be used as tool compounds for drug development, organ toxicity and disease mechanism research.

Indocyanine green 15+ Cited Publications Foxgreen; IC Green; Cardiogreen	Chromogenic Assays
Indocyanine green (Foxgreen) is a low toxicic fluorescent agent that has been widely used in medical diagnostics, such as determining cardiac output, hepatic function, and liver blood flow, and for ophthalmic angiography .

Fasciculin-I FAS-I	Cholinesterase (ChE)	Neurological Disease
Fasciculin-I is isolated from the mambas venom. Fasciculin-I exerts its toxic effects by inhibiting acetylcholinesterase (AChE). Fasciculin-I blocks α-neurotoxins of nicotinic acetylcholine receptors and cardiac toxins that interact with cell membranes .

Cat. No.	Product Name	Category	Target	Chemical Structure