Search Result

Pathways Recommended:	Neuronal Signaling JAK/STAT Signaling

Results for "

biased signaling

" in MedChemExpress (MCE) Product Catalog:

By Targets:	5-HT Receptor (1) Adrenergic Receptor (1) Amyloid-β (1) Angiotensin Receptor (5) Apelin Receptor (APJ) (2) Arrestin (6) Cannabinoid Receptor (1) Cholecystokinin Receptor (2) Dopamine Receptor (4) Epigenetic Reader Domain (1) ERK (2) GABA Receptor (1) GCGR (2) GLP Receptor (2) GPR35 (1) GPR52 (1) GPR84 (1) Hydroxycarboxylic Acid Receptor (HCAR) (1) MMP (1) Neuropeptide Y Receptor (2) Neurotensin Receptor (1) Opioid Receptor (3) Protease Activated Receptor (PAR) (1) Transmembrane Glycoprotein (1)
By Research Areas:	Cancer (1) Cardiovascular Disease (8) Endocrinology (1) Inflammation/Immunology (4) Metabolic Disease (2) Neurological Disease (12)

By Targets:

5-HT Receptor (1)

Adrenergic Receptor (1)

Amyloid-β (1)

Angiotensin Receptor (5)

Apelin Receptor (APJ) (2)

Arrestin (6)

Cannabinoid Receptor (1)

Cholecystokinin Receptor (2)

Dopamine Receptor (4)

Epigenetic Reader Domain (1)

ERK (2)

GABA Receptor (1)

GCGR (2)

GLP Receptor (2)

GPR35 (1)

GPR52 (1)

GPR84 (1)

Hydroxycarboxylic Acid Receptor (HCAR) (1)

MMP (1)

Neuropeptide Y Receptor (2)

Neurotensin Receptor (1)

Opioid Receptor (3)

Protease Activated Receptor (PAR) (1)

Transmembrane Glycoprotein (1)

By Research Areas:

Cancer (1)

Cardiovascular Disease (8)

Endocrinology (1)

Inflammation/Immunology (4)

Metabolic Disease (2)

Neurological Disease (12)

Inhibitors & Agonists

Screening Libraries

Peptides

Targets Recommended: RGS Protein

Cat. No.	상품명	Target	연구분야	Chemical Structure

HY-P2141

TRV-120027 3 Publications Verification TRV027	Angiotensin Receptor Arrestin	Cardiovascular Disease
TRV120027, a *β-arrestin-1*-biased agonist of the angiotensin II receptor type 1 (AT1R), engages β-arrestins while blocking G-protein signaling . TRV120027 induces acute catecholamine secretion through cation channel subfamily C3 (TRPC3) coupling, promotes the formation of a macromolecular complex composed of AT1R-β-arrestin-1-TRPC3-PLCγ at the plasma membrane. TRV120027 inhibits angiotensin II-mediated vasoconstriction and increases cardiomyocyte contractility. TRV120027 has the potential for the acute decompensated heart failure (ADHF) treatment .

HY-128121

MLS1547	Dopamine Receptor	Neurological Disease
MLS1547 is a highly efficacious *G protein-biased* dopamine D2 receptor (D2R) agonist (K_i*=1.2 μM). MLS1547 stimulates D2R G protein-mediated signaling* (EC₅₀=0.37 μM in a calcium mobilization assay). MLS1547 acts as an antagonist for dopamine (DA)-stimulated β-arrestin recruitment to the D2R (IC₅₀=9.9 μM) .

HY-P3137

TRV056	Angiotensin Receptor	Cardiovascular Disease
TRV056 is a Gq-biased ligand of the angiotensin II receptor type 1 (AT1R). TRV056 is efficacious in stimulating cellular Gq-mediated signaling. TRV056 can be used to develop the Gq-biased AT1R agonists .

HY-16642A

LY2828360 1 Publications Verification	Cannabinoid Receptor	Neurological Disease
LY2828360 is a slowly acting but efficacious G protein-biased cannabinoid (CB₂) agonist, inhibiting cAMP accumulation and activating ERK1/2 signaling.

HY-171978

LM-189	Adrenergic Receptor	Cardiovascular Disease
LM-189 is a β₂-adrenergic receptor (β₂AR) ligand and G protein-biased modulator with a human β₂AR K_i of 0.063 nM.LM-189 promotes β₂AR coupling to Gαs and Gαi heterotrimers, stabilizes distinct β₂AR conformations including a TM6 outward state, and increases β₂AR ICL2 dynamics.LM-189 restricts β₂AR ligand-binding pocket conformational heterogeneity, stabilizes polar ligand-receptor interaction networks, and exhibits bias toward Gαi signaling over Gαs signaling.LM-189 enabled cryo-EM structural characterization of the β₂AR-Gi complex.LM-189 can be used for the research of congestive heart failure .

HY-111385

UNC9994 hydrochloride 2 Publications Verification	Dopamine Receptor 5-HT Receptor Arrestin	Neurological Disease
UNC9994 hydrochloride is a functionally selective, *β-arrestin–biased* dopamine D₂ receptor (D₂R) agonist that selectively activates β-arrestin recruitment and signaling. UNC9994 hydrochloride shows a binding affinity with a K_i of 79 nM for D₂R. UNC9994 hydrochloride is also an antagonist of G_i-regulated cAMP production and partial agonist for D2R/β-arrestin-2 interactions. UNC9994 hydrochloride shows antipsychotic-like activity .

HY-120511

KNT-127 1 Publications Verification	Opioid Receptor	Neurological Disease
KNT-127 is a selective and BBB-penetrant δ-opioid receptor (DOR) agonist (K_i = 0.16 nM). KNT-127 is highly selective to the δ receptor, with Ki values of 0.16, 21.3 and 153 nM for δ, μ and κ receptors, respectively. KNT-127 acts as a biased ligand that mainly activates cyclic adenosine monophosphate (cAMP) signaling with lower beta-arrestin signaling activation. KNT-127 increases the release of dopamine and L-glutamate in the striatum, nucleus accumbens, and prefrontal cortex. KNT-127 exhibits antidepressant- and anxiolytic-like effects. KNT-127 can be studied in research on neurological diseases .

HY-16639

ML314	GPR35 Neurotensin Receptor	Neurological Disease Endocrinology
ML314 is a potent, BBB-penetrant and β-arrestin biased molecule agonist of NTR1 (EC₅₀ = 1.9 μM). ML314 shows good selectivity against NTR2 and GPR35, but does not stimulate Ca2+ mobilization. ML314 can attenuate amphetamine-like hyperlocomotion in dopamine transporter knockout mice. ML314 attenuates methamphetamine-associated hyperlocomotion and potentiates the psychostimulant inhibitory effects of a ghrelin antagonist in wild type mouse model. ML314 also acts as an allosteric enhancer of endogenous neurotensin. ML314 antagonizes G protein signaling. ML314 can be studied in research for methamphetamine abuse conditions .

HY-P3136

TRV055 TRV120055	Angiotensin Receptor ERK	Cardiovascular Disease
TRV055 (TRV120055) is a G protein-biased agonist of angiotensin II type 1 receptors (AT1Rs). TRV120055 induces fibroblast proliferation, overexpression of collagen I and α-SMA, and stress fibre formation in human cardiac fibroblasts. TRV055 activates AT1 receptor/Gαq-mediated signaling pathways, upregulates TGF-β1 and p-ERK1/2. TRV055 induces collagen secretion in adult rat myofibroblasts at a level comparable to Ang II. TRV055 can be used to study the role of G protein-biased signaling of AT1Rs in regulating fibrotic responses ^[1]

HY-120920

UNC9995	Dopamine Receptor	Inflammation/Immunology
UNC9995 is a β-arrestin2-biased agonist of dopamine receptor Drd2. UNC9995 inhibits NLRP3 inflammasome activation by enhancing β-arrestin2-NLRP3 interaction, thus prevents neuronal degeneration. Futhermore, UNC9995 activates the Drd2/β-arrestin2 signaling to prevent inflammation-related genes transcription-induced by JAK/STAT3. UNC9995 improves depressive behavior in mouse model, and improves astrocytes dysfunctions .

HY-103475

GS39783	GABA Receptor	Neurological Disease
GS39783 is a positive allosteric modulator (PAM) of GABA_BR. Positive modulation of the GABA_BR can be used for the research of Nicotine addiction .

HY-P3136A

TRV055 hydrochloride TRV120055 hydrochloride	Angiotensin Receptor	Cardiovascular Disease
TRV055 (TRV120055) hydrochloride is a G protein-biased agonist of angiotensin II type 1 receptors (AT1Rs). TRV055 hydrochloride induces fibroblast proliferation, overexpression of collagen I and α-SMA, and stress fibre formation in human cardiac fibroblasts. RV055 hydrochloride activates AT1 receptor/Gαq-mediated signaling pathways, upregulates TGF-β1 and p-ERK1/2. RV055 hydrochloride induces collagen secretion in adult rat myofibroblasts at a level comparable to Ang II. RV055 hydrochloride can be used to study the role of G protein-biased signaling of AT1Rs in regulating fibrotic responses ^[1]

HY-163671

PW0729	GPR52 Arrestin	Neurological Disease
PW0729 is a selective GPR52 agonist. PW0729 activates G protein/cAMP signaling pathway, with bias toward this pathway over β-arrestin recruitment, and induces GPR52 desensitization. PW0729 can be used for the research of neuropsychiatric and neurological diseases .

HY-156025

HCAR2 agonist 1	Hydroxycarboxylic Acid Receptor (HCAR)	Inflammation/Immunology
HCAR2 agonist 1 (Compound 9n) is a G_i protein-biased allosteric modulator of HCAR2. HCAR2 agonist 1 activates the G_i protein signaling pathway. HCAR2 agonist 1 shows anti-inflammatory effect, and reduces mRNA level of pro-inflammatory cytokine (TNF-α, IL-1β, IL-6, and MCP-1). HCAR2 agonist 1 enhances anti-inflammatory effects of orthosteric agonists in the mouse model of colitis .

HY-110302

6'-GNTI dihydrochloride	Opioid Receptor	Neurological Disease
6'-GNTI dihydrochloride, a κ-opioid receptor (KOR) agonist, displays bias toward the activation of G protein-mediated signaling over β-arrestin2 recruitment. 6'-GNTI 6'-GNTI dihydrochloride only activates the Akt pathway in striatal neurons .

HY-P2141A

TRV-120027 TFA 3 Publications Verification	Angiotensin Receptor Arrestin	Cardiovascular Disease
TRV120027 TFA, a *β-arrestin-1*-biased agonist of the angiotensin II receptor type 1 (AT1R), engages ?-arrestins while blocking G-protein signaling . TRV120027?TFA induces?acute?catecholamine?secretion?through cation channel subfamily C3 (TRPC3) coupling, promotes the formation of a macromolecular complex composed of AT1R–β-arrestin-1–TRPC3–PLCγ at the plasma membrane. TRV120027 TFA inhibits angiotensin II–mediated vasoconstriction and increases cardiomyocyte contractility. TRV120027 TFA has the potential for the?acute decompensated heart failure (ADHF) treatment .

HY-P11540

CCKBR agonist-1	Cholecystokinin Receptor MMP Amyloid-β	Neurological Disease
CCKBR agonist-1 (Compound 3r1) is a Gq-protein-preferring cholecystokinin B receptor (CCKBR) agonist with an EC₅₀ of 35 pM. CCKBR agonist-1 significantly increases the survival rate of neurons, with an EC₅₀ of 37 pM. CCKBR agonist-1 can improve the cognitive decline in mice by upregulating α-secretase (ADAM10) and calcium signaling molecule PLCB4, reduce the number of amyloid β (Aβ) plaques, and promote long-term potentiation (LTP). CCKBR agonist-1 can be used for the study of Alzheimer's disease .

HY-P3347

NH2-c[X-R-L-S-X]-K-G-P-(D-2Nal)	Apelin Receptor (APJ)	Cardiovascular Disease
NH2-c[X-R-L-S-X]-K-G-P-(D-2Nal) (compound 40), a macrocyclic analogue of Ape13, is a potent APJ agonist (K_i=5.7 nM). NH2-c[X-R-L-S-X]-K-G-P-(D-2Nal) exhibits a favorable Gα12-biased signaling and an increased in vivo half-life .

HY-161107

OX04529	GPR84	Inflammation/Immunology
OX04529 (compound 69) is a potent, selective and orally active agonist of GPR84. OX04529 inhibits FSK-induced cAMP production with an EC₅₀ of 0.0185 nM. OX04529 displayed excellent potency, high G-protein signaling bias .

HY-P3259

AY254	Protease Activated Receptor (PAR)	Inflammation/Immunology Cancer
AY254 is an analogue of AY77 (HY-138951). AY254 is ERK-biased PAR2 agonist with an EC₅₀ of 2 nM. AY254 relieves cytokine-induced caspase 3/8 activation. AY254 also promotes scratch-wound healing and induced IL-8 secretion via PAR2-ERK1/2 signaling

HY-P11275

TC4	GLP Receptor GCGR Neuropeptide Y Receptor	Metabolic Disease
TC4 is a highly balanced single-molecule quadruple agonist that can respectively activate GIPR, GLP-1R, GcgR, and Y2R with IC₅₀ values of 0.95, 31, 81, and 1100 nM respectively. TC4 exhibits extremely strong signal bias on GLP-1R and has very low recruitment efficacy for β-inhibitor protein 2 (βArr2) and this strong cAMP preference is believed to maximize metabolic benefits (such as weight loss and hypoglycemia) while possibly minimizing side effects mediated by β-inhibitor protein recruitment (such as receptor desensitization). TC4 can be used for research on obesity and diabetes .

HY-161812

MOR agonist-4	Opioid Receptor	Others
MOR agonist-4 (2d) is a G protein signaling-biased Kappa opioid receptor (KOR) agonist with an EC₅₀ value of 11 nM. MOR agonist-4 contains an electron withdrawing CF3 group and a bias factor of 38 based on triazole. MOR agonist-4 is used in the research of pruritis and analgesia .

HY-116445

UNC9975	Dopamine Receptor	Neurological Disease
UNC9975 is a D₂R agonist that displays signaling bias via β-arrestin–ergic signaling and a simultaneously antagonist of Gi-regulated cAMP production and partial agonist for D₂R/β-arrestin-2 interactions. UNC9975 can be utilized in antipsychotic research .

HY-P11279

TC2	GLP Receptor GCGR Neuropeptide Y Receptor	Metabolic Disease
TC2 is an efficient GIPR-preferring monomeric quadruple agonist that can respectively activate GIPR, GLP-1R, GcgR, and Y2R with IC₅₀ values of 0.47, 2.1, 30, and 55 nM respectively. TC2 exhibits a significant GLP-1R preference, with a significant reduction in β-inhibitory protein 2 (βArr2) recruitment, while maintaining a strong cAMP signal. TC2 can be used for research on obesity and diabetes .

HY-183777

B-007	Apelin Receptor (APJ) Arrestin	Cardiovascular Disease
B-007 is an AplnR agonist with G protein-biased signaling (EC₅₀ = 11.6 nM). B-007 activates the G protein pathway while abolishing β-arrestin1 and β-arrestin2 signaling. B-007 serves as a scaffold for development of G protein-biased apelin receptor agonists. B-007 can be used for the research of heart failure .

HY-179606

RWT9996	Transmembrane Glycoprotein Arrestin ERK Epigenetic Reader Domain	Neurological Disease
RWT9996 is a balanced GPR17 antagonist. RWT9996 has an inhibitory effect on G protein activation and β-arrestin-2 recruitment induced by MDL-29951. RWT9996 inhibits the phosphorylation of ERK/CREB and the accumulation of inositol phosphate (b IP1) induced by MDL-29951. RWT9996 can be used for the study of neurological diseases .

HY-179721

CCKBR agonist-2	Cholecystokinin Receptor	Neurological Disease
CCKBR agonist-2 (Compound z-44) is a Gi-preferring CCKBR agonist. CCKBR agonist-2 effectively activates the CCKBR-Gi signaling pathway (EC₅₀ = 0.27 nM), but has almost no activity on Gq and Gs signaling pathways. CCKBR agonist-2 shows no significant protective effect in the mouse Alzheimer's disease model, proving that the simple activation of the Gi signal pathway does not play a dominant role in the improvement of cognitive function .

Cat. No.	상품명

HY-L170

Allosteric Modulators (AMs) Compound Library	250 compounds
An emerging drug design method is based on the secondary binding site effect, where small molecule drugs are designed to bind to secondary binding sites on target biomolecules rather than primary orthomorphic sites. Successful potential drugs (known as allosteric modulators) will be able to bind to allosteric sites and remotely alter (or modify) the conformation of the main orthosteric binding sites of biological targets. Allosteric modulators (AMs) are ligands of proteins that act through binding sites different from natural (orthosteric) ligand sites. AMs are relatively small, more lipophilic, and more rigid compounds. The binding efficacy of AMs with their targets is often slightly lower. AMs are divided into positive AMs (PAMs) and negative AMs (NAMs). AMs are ideal drug targets because they can fine-tune receptor activity while preserving the spatial and temporal signal transduction characteristics of endogenous ligands, resulting in fewer targeted side effects, improved subtype selectivity, and better promotion of biased signal transduction than normal ligands. MCE designs a unique collection of 250 small allosteric modulators. It is a good tool to be used for research on metabolize, cancer and other diseases.

Allosteric Modulators (AMs) Compound Library

250 compounds

An emerging drug design method is based on the secondary binding site effect, where small molecule drugs are designed to bind to secondary binding sites on target biomolecules rather than primary orthomorphic sites. Successful potential drugs (known as allosteric modulators) will be able to bind to allosteric sites and remotely alter (or modify) the conformation of the main orthosteric binding sites of biological targets. Allosteric modulators (AMs) are ligands of proteins that act through binding sites different from natural (orthosteric) ligand sites. AMs are relatively small, more lipophilic, and more rigid compounds. The binding efficacy of AMs with their targets is often slightly lower. AMs are divided into positive AMs (PAMs) and negative AMs (NAMs). AMs are ideal drug targets because they can fine-tune receptor activity while preserving the spatial and temporal signal transduction characteristics of endogenous ligands, resulting in fewer targeted side effects, improved subtype selectivity, and better promotion of biased signal transduction than normal ligands.

MCE designs a unique collection of 250 small allosteric modulators. It is a good tool to be used for research on metabolize, cancer and other diseases.

Cat. No.	상품명	Target	Research Area