biased

TRV120056 acetate is a Gq-biased agonist with 10-fold greater molecular efficiency on AT1R-Gq fusion proteins than AT1R-βarr2 fusion proteins.

TRV-120027 acetate is a β-arrestin-1-biased agonist of the angiotensin II receptor type 1 (AT1 receptor) and engages -arrestins while blocking G-protein signaling.

Apelin biased agonist; exhibits bias for the G protein pathway. Stimulates endothelial NOS phosphorylation and expression, promotes proliferation, and attenuates apoptosis of human pulmonary arterial endothelial cells in vitro. Shows positive inotropic an

TRV055 is a Gq-biased ligand of the angiotensin II receptor type 1 (AT1R). TRV055 is efficacious in stimulating cellular Gq-mediated signaling. TRV055 can be used to develop the Gq-biased AT1R agonists.

TRV120027 is a β-arrestin-1-biased agonist of the angiotensin II receptor type 1. TRV120027 inhibits angiotensin II-mediated vasoconstriction and increases cardiomyocyte contractility.

TRV120027 TFA is a β-arrestin-1-biased agonist of the angiotensin II receptor type 1 (AT1R) and engages ß-arrestins while blocking G-protein signaling.

Bilaid C is a tetrapeptide μ-opioid receptor agonist (Ki= 210 nM in HEK293 cell membranes expressing the human receptor) that has been found inPenicillium.1It inhibits forskolin-induced cAMP accumulation by 77% in HEK293 cells expressing the human μ-opioid receptor when used at a concentration of 10 μM. Bilaid C induces inward rectifying potassium channel (Kir) currents in rat locus coeruleus slices that endogenously express high levels of the μ-opioid receptor (EC50= 4.2 μM). 1.Dekan, Z., Sianati, S., Yousuf, A., et al.A tetrapeptide class of biased analgesics from an Australian fungus targets the μ-opioid receptorProc. Natl. Acad. Sci. USA116(44)22353-22358(2019)

TRV120056 is a Gq-biased agonist that demonstrates a molecular efficacy ten times greater at the AT1R-Gq fusion protein than at the AT1R-βarr2 fusion protein.

TRV056 is a Gq-biased agonist of the angiotensin II type 1 receptor (AT1R), demonstrating efficacy in stimulating Gq-mediated cellular signaling. It can serve as a foundation for the development of Gq-biased AT1R agonists.

TRV120055, a Gq-biased agonist, demonstrates a 10-fold higher molecular efficacy when tested against the AT1R-Gq fusion protein in comparison to the AT1R-βarr2 fusion protein.

ATI-2341 is an effective functionally selective allosteric agonist for the c-x-c chemokine receptor type 4 (CXCR4), which ACTS as a biased ligand in favor of G G G G G 1 activation instead of G G G G G 13.ATI-2341 activates the inhibitory heterotrimer G p

AY 254 is a potent PAR2 biased agonist. Selectively activates ERK1/2 signaling (EC50= 2 nM for ERK1/2 phosphorylation versus 80 nM for Ca2+release). Reduces cytoKi ne-induced caspase 3/8 activation, promotes scratch-wound healing, and induces IL-8 secretion, in human colorectal cancer (HT29) cellsin vitro.

α-Conotoxin MrIC is a biased agonist selective for the α7 nicotinic acetylcholine receptor (nAChR), with activation contingent upon the presence of type II positive allosteric modulators, such as PNU120596. It is utilized to investigate neurological disorders and delineate the pharmacological characteristics of the α7nAChR [1].

ATI-2341 is a potent, functionally selective allosteric agonist of the C-X-C chemokine receptor type 4 (CXCR4), acting as a biased ligand that prefers Gαi activation over Gα13. This compound activates the inhibitory heterotrimeric G protein (Gi), leading to reduced cAMP production and enhanced calcium mobilization. ATI-2341 effectively mobilizes bone marrow polymorphonuclear neutrophils (PMNs) and hematopoietic stem and progenitor cells (HSPCs) [1] [2].

TRV055 hydrochloride, a Gq-biased ligand and G-protein-biased agonist of the angiotensin II receptor type 1 (AT1R), effectively stimulates cellular Gq-mediated signaling [1].