scholarly journals Development of a human vasopressin V1a-receptor antagonist from an evolutionary-related insect neuropeptide

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Maria Giulia Di Giglio ◽  
Markus Muttenthaler ◽  
Kasper Harpsøe ◽  
Zita Liutkeviciute ◽  
Peter Keov ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
V1a Receptor ◽  
Insect Neuropeptide ◽  
Vasopressin V1a Receptor

Luteolin, a Potent Human Monoamine Oxidase-A Inhibitor and Dopamine D4 and Vasopressin V1A Receptor Antagonist

2020 ◽  
Vol 68 (39) ◽  
pp. 10719-10729
Author(s):  
Se Eun Park ◽  
Pradeep Paudel ◽  
Aditi Wagle ◽  
Su Hui Seong ◽  
Hyeong Rak Kim ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Receptor Antagonist ◽  
Monoamine Oxidase A ◽  
V1a Receptor ◽  
Vasopressin V1a Receptor

scholarly journals Evidence of early vasogenic edema following minor head impact that can be reduced with a vasopressin V1a receptor antagonist

2020 ◽  
Vol 165 ◽  
pp. 218-227
Author(s):  
Praveen Kulkarni ◽  
Mansi R. Bhosle ◽  
Shi-fang Lu ◽  
Neal S Simon ◽  
Sade Iriah ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Vasogenic Edema ◽  
Head Impact ◽  
V1a Receptor ◽  
Vasopressin V1a Receptor

Molecular analysis of antilipemic effects of FR218944, a novel vasopressin V1a receptor antagonist, in genetically diabetic db/db mice in comparison with pioglitazone and fenofibrate

2003 ◽  
Vol 60 (4) ◽  
pp. 241-251 ◽  
Author(s):  
Masahiko Morita ◽  
Akiko Ohkubo-Suzuki ◽  
Tokiko Takahashi ◽  
Akira Nagashima ◽  
Yuki Sawada ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Molecular Analysis ◽  
V1a Receptor ◽  
Vasopressin V1a Receptor

Potent Inhibitory Effect of Sr 49059, An Orally Active Non-Peptide Vasopressin via Receptor Antagonist, on Human Arterial Coronary Bypass Graft

1995 ◽  
Vol 89 (5) ◽  
pp. 481-485 ◽  
Author(s):  
James J. Liu ◽  
Joan R. Chen ◽  
Brian B. Buxton ◽  
Colin I. Johnston ◽  
Louise M. Burrell
Keyword(s):  
Receptor Antagonist ◽  
Bypass Graft ◽  
Coronary Bypass ◽  
Inhibitory Effect ◽  
V1a Receptor ◽  
Mammary Arteries ◽  
Coronary Bypass Graft ◽  
Internal Mammary ◽  
Vasopressin V1a Receptor

1. The effect of vasopressin receptor antagonists varies between analogues (peptide, non-peptide) and across species. In this study the effect of the novel non-peptide vasopressin V1a receptor antagonist SR 49059 on human internal mammary arteries was investigated. 2. SR 49059 produced a potent, concentration-dependent, inhibitory effect on vasopressin-induced contraction of human coronary bypass graft internal mammary arteries. Both SR 49059 (1 μmol/l) and a peptide selective V1a antagonist {[d(CH2)5sarcosine7]arginine vasopressin} (1 μmol/l) abolished vasopressin-induced contraction. The non-peptide V1a receptor antagonist OPC-21268 (1 μmol/l) had no effect on vasopressin-induced contraction. 3. The effect of SR 49059 was specific to vascular vasopressin receptors as noradrenaline-induced contraction was not influenced by SR 49059. 4. The results of this study in vitro indicate that the non-peptide SR 49059 is a potent, specific vasopressin V1a receptor antagonist in the human internal mammary artery and suggest that it may be a useful tool for studying the pathophysiological role of vasopressin in man.

A nonpeptide vasopressin V1a receptor antagonist, SR 49059, does not prevent cisplatin-induced emesis in piglets

2001 ◽  
Vol 15 (3) ◽  
pp. 189-200 ◽  
Author(s):  
Laurent Grelot ◽  
Vincent Girod ◽  
Julien Dapzol ◽  
Jean Pierre Maffrand ◽  
Claudine Serradeil-Le Gal
Keyword(s):  
Receptor Antagonist ◽  
V1a Receptor ◽  
Vasopressin V1a Receptor

A phase 2 clinical trial of a vasopressin V1a receptor antagonist shows improved adaptive behaviors in men with autism spectrum disorder

2019 ◽  
Vol 11 (491) ◽  
pp. eaat7838 ◽  
Author(s):  
Federico Bolognani ◽  
Marta del Valle Rubido ◽  
Lisa Squassante ◽  
Christoph Wandel ◽  
Michael Derks ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Autism Spectrum Disorder ◽  
Receptor Antagonist ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Social Responsiveness ◽  
Phase 2 ◽  
V1a Receptor ◽  
Phase 2 Clinical Trial ◽  
Vasopressin V1a Receptor

There are no approved pharmacological therapies to address the core symptoms of autism spectrum disorder (ASD), namely, persistent deficits in social communication and social interaction and the presence of restricted, repetitive patterns of behaviors, interests, or activities. The neuropeptide vasopressin has been implicated in the regulation of social behaviors, and its modulation has emerged as a therapeutic target for ASD. The phase 2 VANILLA clinical trial reported here evaluated balovaptan, an orally administered selective vasopressin V1a receptor antagonist, in 223 men with ASD and intelligence quotient ≥70. The drug was administered daily for 12 weeks and was compared with placebo. Participants were randomized to placebo (n = 75) or one of three balovaptan dose arms (1.5 mg, n = 32; 4 mg, n = 77; 10 mg, n = 39). Balovaptan treatment was not associated with a change from baseline compared with placebo at 12 weeks in the primary efficacy endpoint (Social Responsiveness Scale, 2nd Edition). However, dose-dependent and clinically meaningful improvements on the Vineland-II Adaptive Behavior Scales composite score were observed for participants treated with balovaptan 4 or 10 mg compared with placebo. This was driven principally by improvements in the Vineland-II socialization and communication scores. Balovaptan was well tolerated across all doses, and no drug-related safety concerns were identified. These results support further study of balovaptan as a potential treatment for the socialization and communication deficits in ASD.

scholarly journals Evidence of Early Vasogenic Edema Following Minor Head Injury That Can Be Reduced With a Vasopressin V1a Receptor Antagonist

2020 ◽  
Author(s):  
Praveen Kulkarni ◽  
Mansi R Bhosle ◽  
Shi-fang Lu ◽  
Sade Iriah ◽  
Neal G. Simon ◽  
...  
Keyword(s):  
Head Injury ◽  
Receptor Antagonist ◽  
Vasogenic Edema ◽  
Brain Regions ◽  
Minor Head Injury ◽  
Male Rats ◽  
Momentum Exchange ◽  
Brain Areas ◽  
V1a Receptor ◽  
Vasopressin V1a Receptor

Abstract Background: Does minor head injury without signs of structural brain damage cause short-term changes in vasogenic edema as measured by an increased apparent diffusion coefficient (ADC) using diffusion weighted imaging? If so, could the increase in vasogenic edema be treated with a vasopressin V1a receptor antagonist? We hypothesized that SRX251, a highly selective V1a antagonist, would reduce vasogenic edema in response to a single minor head injury.Methods: Lightly anesthetized male rats were subjected to a sham procedure or a single hit to the forehead using a closed skull, momentum exchange model. Animals recovered in five min and were injected with saline vehicle (n=8) or SRX251 (n=8) at 15 min post head injury and again 7-8 hrs later. At 2 hrs, 6 hrs, and 24 hrs post injury, rats were anesthetized and scanned for increases in ADC, a neurological measure of vasogenic edema. Sham rats (n=6) were exposed to anesthesia and scannedat all time points but were not hit or treated. Images were registered to and analyzed using a 3D MRI rat atlas providing site-specific data on 150 different brain areas. These brain areas were divided into 11 major brain regions.Results: Untreated rats with head injury showed a significant increase in global brain vasogenic edema as compared to sham and SRX251 treated rats. Edema peaked at 6 hrs in injured, untreated rats in three brain regions where changes in ADC were observed, but returned to sham levels by 24 hrs. There were regional variations in the time course of vasogenic edema and drug efficacy. Edema was significantly reduced in cerebellum and thalamus with SRX251 treatment while the basal ganglia did not show a significant response to treatment. Conclusion: A single minor impact to the forehead causes regional increases in vasogenic edema that peak at 6 hrs but return to baseline within a day in a subset of brain regions. Treatment with a selective V1a receptor antagonist can reduce much of the edema.

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