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Results for "

withdrawal

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Adrenergic Receptor (5) Apoptosis (1) Calcium Channel (1) CRFR (2) Cyclic GMP-AMP Synthase (1) ERK (1) Isotope-Labeled Compounds (1) Melatonin Receptor (3) mGluR (1) nAChR (1) Opioid Receptor (6) PKA (2) Sodium Channel (1)
By Research Areas:	Cancer (6) Cardiovascular Disease (3) Endocrinology (9) Metabolic Disease (2) Neurological Disease (17)

Inhibitors & Agonists

Screening Libraries

Peptides

Isotope-Labeled Compounds

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-A0142A

Dapiprazole hydrochloride	Adrenergic Receptor	Endocrinology
Dapiprazole hydrochloride is a potent, selective and orally active alpha-1 adrenoceptor antagonist. Dapiprazole hydrochloride suppresses the opioid withdrawal symptoms. Dapiprazole hydrochloride is also used as eye drops for reversing mydriasis .

HY-A0014

Ramelteon Maximum Cited Publications 7 Publications Verification TAK-375	Melatonin Receptor	Neurological Disease Endocrinology Cancer
Ramelteon is a potent, highly selective, and orally active agonist of MT1/MT2 with Ki values of 14 and 112 pM, respectively. Ramelteon has the potential for the research of insomnia. Ramelteon consistently reduces sleep onset after long-term treatment, with no next-morning residual effects or rebound insomnia or withdrawal symptoms upon discontinuation .

HY-A0142

Dapiprazole	Adrenergic Receptor	Endocrinology
Dapiprazole is a potent, selective and orally active alpha-1 adrenoceptor antagonist. Dapiprazole suppresses the opioid withdrawal symptoms. Dapiprazole is also used as eye drops for reversing mydriasis .

HY-144608

Mu opioid receptor antagonist 3	Opioid Receptor	Neurological Disease
Mu opioid receptor antagonist 3 (compound 26) is a potent and selective μ opioid receptor (MOR) antagonist with a K_i of 0.24 nM and an EC₅₀ of 0.54 nM. Mu opioid receptor antagonist 3 has remarkable CNS antagonism against morphine, and precipitated fewer withdrawal symptoms than Naloxone. Mu opioid receptor antagonist 3 can be used for researching opioid use disorders (OUD) .

HY-144609

Mu opioid receptor antagonist 4	Opioid Receptor	Neurological Disease
Mu opioid receptor antagonist 4 (compound 31) is a potent and selective μ opioid receptor (MOR) antagonist with a K_i of 0.38 nM and an EC₅₀ of 1.07 nM. Mu opioid receptor antagonist 4 has remarkable CNS antagonism against morphine, and precipitated fewer withdrawal symptoms than Naloxone. Mu opioid receptor antagonist 4 Mu opioid receptor antagonist 4 can be used for researching opioid use disorders (OUD) .

HY-144607

Mu opioid receptor antagonist 2	Opioid Receptor	Neurological Disease
Mu opioid receptor antagonist 2 (compound 25) is a potent, selective and blood-brain barrier (BBB) penetrant μ opioid receptor (MOR) antagonist with a K_i of 0.37 nM and an EC₅₀ of 0.44 nM. Mu opioid receptor antagonist 2 has remarkable CNS antagonism against morphine, and precipitated fewer withdrawal symptoms than Naloxone. Mu opioid receptor antagonist 2 can be used for researching opioid use disorders (OUD) .

HY-A0014R

Ramelteon (Standard)	Melatonin Receptor	Neurological Disease Endocrinology Cancer
Ramelteon (Standard) is the analytical standard of Ramelteon. This product is intended for research and analytical applications. Ramelteon is a potent, highly selective, and orally active agonist of MT1/MT2 with Ki values of 14 and 112 pM, respectively. Ramelteon has the potential for the research of insomnia. Ramelteon consistently reduces sleep onset after long-term treatment, with no next-morning residual effects or rebound insomnia or withdrawal symptoms upon discontinuation .

HY-B1052S

Lofexidine-d4 hydrochloride	Adrenergic Receptor	Neurological Disease Endocrinology
Lofexidine-d₄ (hydrochloride) (Baq-168-d4) is the deuterium labeled Lofexidine hydrochloride. Lofexidine hydrochloride is a selective α2-receptor agonist, commonly used to alleviate the physical symptoms of heroin and other types of opioid withdrawal[1][2].

HY-B1052

Lofexidine hydrochloride Baq-168; MDL-14042	Adrenergic Receptor	Neurological Disease Endocrinology
Lofexidine (hydrochloride) is a selective α2-receptor agonist, commonly used to alleviate the physical symptoms of heroin and other types of opioid withdrawal .

HY-B1052A

Lofexidine	Adrenergic Receptor	Neurological Disease Endocrinology
Lofexidine is a selective α2-receptor agonist, commonly used to alleviate the physical symptoms of heroin and other types of opioid withdrawal .

HY-14127

R121919 2 Publications Verification NBI30775	CRFR	Neurological Disease Endocrinology
R121919 (NBI30775) is a potent and selective CRF1R antagonist with a K_i of 2 to 5 nM. R121919 has antidepressant and anxiolytic effects. R121919 alleviates defensive withdrawal in rats .

HY-115645

R121919 hydrochloride NBI30775 hydrochloride	CRFR	Neurological Disease Metabolic Disease
R121919 (NBI30775) hydrochloride is a potent and selective CRF1R antagonist with a K_i of 2 to 5 nM. R121919 hydrochloride has antidepressant and anxiolytic effects. R121919 hydrochloride alleviates defensive withdrawal in rats .

HY-104006

CYM51010	Opioid Receptor	Neurological Disease
CYM51010 is a biased ligand of μ-opioid receptor – δ-opioid receptor heterodimers with an EC₅₀ of 403 nM. CYM51010 exhibits anti-nociceptive activity similar to morphine but with a decreased levels of tolerance development and withdrawal symptoms .

HY-100781B

L-AP4 monohydrate L-APB monohydrate	mGluR	Neurological Disease
L-AP4 (L-APB) monohydrate is a potent and specific agonist for the group III mGluRs, with EC₅₀s of 0.13, 0.29, 1.0, 249 μM for mGlu₄, mGlu₈, mGlu₆ and mGlu₇ receptors, respectively .

HY-151811

NAQ	Opioid Receptor	Neurological Disease
NAQ is a potent and selective μ opioid receptor partial agonist, with a K_i of 0.55 nM. NAQ shows selectivity for Mu opioid receptor over the δ receptor (K_i=132.50 nM) and the κ receptor (K_i=26.45 nM). NAQ can be used for the research of opioid withdrawal or dependence .

HY-129079

TFMB-(R)-2-HG 1 Publications Verification	Others	Cancer
TFMB-(R)-2-HG, a cell membrane-permeable version of (R)-2-HG, is a carcinogenic factor in Acute myeloid leukemia (AML). TFMB-(R)-2-HG impairs SCF ER-Hoxb8 cells differentiation in response to estrogen withdrawal .

HY-156694

Hydroxy-PP-Me	Apoptosis	Cancer
Hydroxy-PP-Me is a potent and specific CBR1 inhibitor with an IC₅₀ of 759 nM. Hydroxy-PP-Me inhibits serum-withdrawal-induced apoptosis. Hydroxy-PP-Me increases As₂O₃-induced apoptotic cell death compared with As₂O₃ alone .

HY-106234

ZP 120C	Opioid Receptor	Cardiovascular Disease Neurological Disease
ZP 120C is a potent and partial ORL1 receptor agonist. ZP 120C inhibits electrically induced contraction. ZP 120C can be used in the research of hyponatremia/hypokalemia .

HY-123468

HA-1004	Cyclic GMP-AMP Synthase PKA ERK Calcium Channel	Cardiovascular Disease Metabolic Disease
HA-1004 is a selective inhibitor of PKA, which can inhibit lipolysis and induce vascular relaxation. HA-1004 is also a dual inhibitor of cyclic GMP-dependent protein kinase and cyclic AMP-dependent protein, and is involved in smooth muscle, second messenger, cyclic AMP and cyclic GMP regulation mechanisms. HA-1004 is an antagonist for calcium, that can be used as a vasodilator to inhibit the contraction of rabbit aortic strips, or to antagonize ERK and tyrosine hydroxylase (TH) phosphorylation in morphine abstinence rat models .

HY-A0014S

Ramelteon-d5 TAK-375-d₅	Isotope-Labeled Compounds Melatonin Receptor	Neurological Disease Endocrinology Cancer
Ramelteon-d₅ is deuterium labeled Ramelteon. Ramelteon is a potent, highly selective, and orally active agonist of MT1/MT2 with Ki values of 14 and 112 pM, respectively. Ramelteon has the potential for the research of insomnia. Ramelteon consistently reduces sleep onset after long-term treatment, with no next-morning residual effects or rebound insomnia or withdrawal symptoms upon discontinuation[1][2].

HY-14565

Pozanicline ABT-089	nAChR	Neurological Disease
Pozanicline (ABT-089) selectively activate neuronal nicotinic acetylcholine receptor (nAChR) subtypes, is a novel cholinergic agent that is a partial agonist at α4β2* nAChRs (K_i=16 nM) and shows high selectivity for α6β2* and α4α5β2 nAChR subtypes, the binding affinity (K_i, rat) for Pozanicline to [ ³H] cytisine sites is 16.7 nM. Pozanicline reverses nicotine withdrawal-induced cognitive deficits, may be an effective component of novel therapeutic strategies for nicotine addiction .

HY-P1441A

Mambalgin 1 TFA	Sodium Channel
Mambalgin 1 TFA is a selective ASIC1a inhibitor (IC₅₀ values are 192 and 72 nM for human ASIC1a and ASIC1a/1b dimer, respectively). Mambalgin 1 TFA binds to closed/inactive channel. Mambalgin 1 TFA is selective for ASIC1a over ASIC2a, ASIC3, TRPV1, P2X2, 5-HT3, Nav1.8, Cav3.2 and Kv1.2 channels. Mambalgin 1 TFA increases latency of withdrawal response in mouse tail-flick and paw-flick tests.

HY-P10319

RI-STAD-2	PKA	Cardiovascular Disease Cancer
RI-STAD-2 is a high-affinity interfering peptide that regulates the subunit RI of protein kinase A (PKA). RI-STAD-2 interferes with the binding of AKAPs and PKA-RI by simulating the interaction between AKAPs' α-helix domain and PKA-RI's dimerization/anchoration (D/D) domain, thereby affecting PKA activity and intracellular localization. RI-STAD-2 can be used to study the role of AKAPs interaction with PKA-RI in pathological processes such as cardiovascular disease and cancer .

Cat. No.	Product Name

HY-L140

Withdrawn Drug Compound Library	199 compounds
Withdrawal or delisting drugs refer to drugs that are recalled or discontinued from the market due to low efficiency, serious side effects, financial and regulatory problems and other reasons. Once the drug is withdrawn from the market, it will cause heavy losses to the original research company that invested a lot of time, finance and other costs to develop the drug. Adverse drug reaction (ADR) is the main reason for drug withdrawal from the market. ADR refers to the unexpected effects caused by the reasons such as the target-directed interaction during the treatment. However, studying the mechanism of these ADRs may just be a breakthrough in finding new indications. For example, thalidomide, the protagonist of the drug damage event that caused numerous "seal babies" deformed infants, was found to be due to the degradation of a transcription factor - SALL4 after delisting, which made thalidomide have a new clinical application. In 1998, it was approved by FDA for the treatment of leprosy nodular erythema, and in 2006, it was approved for the treatment of multiple myeloma. ADR study of delisted drugs can not only avoid the loss of drug development in advance but also bring hope to new indications. MCE has sorted out 199 drug compounds withdrawn from the market through FDA, EMA and other authoritative platforms. Each compound has withdrawal records in at least one country/market. It is a useful tool for conducting research on drug side effects or drug toxicity mechanisms and discovering new indications of drugs.

Withdrawn Drug Compound Library

199 compounds

Withdrawal or delisting drugs refer to drugs that are recalled or discontinued from the market due to low efficiency, serious side effects, financial and regulatory problems and other reasons. Once the drug is withdrawn from the market, it will cause heavy losses to the original research company that invested a lot of time, finance and other costs to develop the drug.

Adverse drug reaction (ADR) is the main reason for drug withdrawal from the market. ADR refers to the unexpected effects caused by the reasons such as the target-directed interaction during the treatment. However, studying the mechanism of these ADRs may just be a breakthrough in finding new indications. For example, thalidomide, the protagonist of the drug damage event that caused numerous "seal babies" deformed infants, was found to be due to the degradation of a transcription factor - SALL4 after delisting, which made thalidomide have a new clinical application. In 1998, it was approved by FDA for the treatment of leprosy nodular erythema, and in 2006, it was approved for the treatment of multiple myeloma. ADR study of delisted drugs can not only avoid the loss of drug development in advance but also bring hope to new indications.

MCE has sorted out 199 drug compounds withdrawn from the market through FDA, EMA and other authoritative platforms. Each compound has withdrawal records in at least one country/market. It is a useful tool for conducting research on drug side effects or drug toxicity mechanisms and discovering new indications of drugs.

HY-L076

Drug-Induced Liver Injury (DILI) Compound Library	1,392 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 1,392 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

1,392 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 1,392 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.

Cat. No.	Product Name	Target	Research Area

HY-P3628

Dynorphin (2-17) (porcine)	Peptides	Neurological Disease
Dynorphin (2-17) (porcine) is a peptide derived from Prodynorphin, can improve somatic signs of Morphine-dependent withdrawal .

HY-106234

ZP 120C	Opioid Receptor	Cardiovascular Disease Neurological Disease
ZP 120C is a potent and partial ORL1 receptor agonist. ZP 120C inhibits electrically induced contraction. ZP 120C can be used in the research of hyponatremia/hypokalemia .

HY-P1441A

Mambalgin 1 TFA	Sodium Channel
Mambalgin 1 TFA is a selective ASIC1a inhibitor (IC₅₀ values are 192 and 72 nM for human ASIC1a and ASIC1a/1b dimer, respectively). Mambalgin 1 TFA binds to closed/inactive channel. Mambalgin 1 TFA is selective for ASIC1a over ASIC2a, ASIC3, TRPV1, P2X2, 5-HT3, Nav1.8, Cav3.2 and Kv1.2 channels. Mambalgin 1 TFA increases latency of withdrawal response in mouse tail-flick and paw-flick tests.

HY-P10319

RI-STAD-2	PKA	Cardiovascular Disease Cancer
RI-STAD-2 is a high-affinity interfering peptide that regulates the subunit RI of protein kinase A (PKA). RI-STAD-2 interferes with the binding of AKAPs and PKA-RI by simulating the interaction between AKAPs' α-helix domain and PKA-RI's dimerization/anchoration (D/D) domain, thereby affecting PKA activity and intracellular localization. RI-STAD-2 can be used to study the role of AKAPs interaction with PKA-RI in pathological processes such as cardiovascular disease and cancer .

Lofexidine-d4 hydrochloride
Lofexidine-d₄ (hydrochloride) (Baq-168-d4) is the deuterium labeled Lofexidine hydrochloride. Lofexidine hydrochloride is a selective α2-receptor agonist, commonly used to alleviate the physical symptoms of heroin and other types of opioid withdrawal[1][2].

Ramelteon-d5
Ramelteon-d₅ is deuterium labeled Ramelteon. Ramelteon is a potent, highly selective, and orally active agonist of MT1/MT2 with Ki values of 14 and 112 pM, respectively. Ramelteon has the potential for the research of insomnia. Ramelteon consistently reduces sleep onset after long-term treatment, with no next-morning residual effects or rebound insomnia or withdrawal symptoms upon discontinuation[1][2].

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