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N- cyclobutyl- 6- ((3- fluorophenyl)ethynyl)nicotinamide

an mGlu5 agonist; structure in first source

Also Known As:

VU0360172

Networked: 14 relevant articles (1 outcomes, 2 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Heterocyclic Compounds: 198
- 1-Ring Heterocyclic Compounds
  - Pyridines: 88
    - Nicotinic Acids: 13
      - Niacinamide: 2223
        N-cyclobutyl-6-((3-fluorophenyl)ethynyl)nicotinamide: 14
- Heterocyclic Acids
  - Nicotinic Acids: 13
    - Niacinamide: 2223
      - N-cyclobutyl-6-((3-fluorophenyl)ethynyl)nicotinamide: 14

Experts

1.	Nicoletti, Ferdinando: 4 articles (11/2020 - 11/2013)
2.	van Luijtelaar, Gilles: 3 articles (11/2020 - 07/2015)
3.	Ngomba, Richard T: 2 articles (01/2022 - 11/2020)
4.	Wall, Mark J: 2 articles (01/2022 - 11/2020)
5.	Cannella, Milena: 2 articles (11/2020 - 11/2013)
6.	Mascio, Giada: 2 articles (11/2020 - 11/2013)
7.	Santolini, Ines: 2 articles (11/2020 - 07/2016)
8.	D'Amore, Valerio: 2 articles (07/2016 - 07/2015)
9.	Ngomba, Richard Teke: 2 articles (07/2016 - 07/2015)
10.	Ji, Guangchen: 2 articles (01/2016 - 02/2014)

Related Diseases

1.	Seizures (Absence Seizure) 03/01/2013 - "Potentiation of mGlu5 receptors with the novel enhancer, VU0360172, reduces spontaneous absence seizures in WAG/Rij rats." 07/01/2015 - "Intrathalamic co-injections of VU0360172 and subthreshold doses of tiagabine caused an antiabsence effect similar to that exhibited by VU0360172 alone in the first 10 min. At 30 min, however, the antiabsence effect of VU0360172 was prevented by subthreshold doses of tiagabine, and the combination produced a paradoxical proabsence effect at 40 and 50 min. These data (1) show that mGlu1 and mGlu5 receptor PAMs reduce absence seizures acting at both thalamic and cortical levels; (2) demonstrate for the first time that tiagabine, despite its established absence-enhancing effect, reduces SWDs when injected into the somatosensory cortex; and (3) indicate that the efficacy of VU0360172 in the thalamus may be critically affected by the availability of (extra)synaptic GABA."
2.	Absence Epilepsy (Childhood Absence Epilepsy) 11/01/2020 - "Previous studies have shown that injection of the mGlu5 receptor positive allosteric modulator (PAM) VU0360172 into either the thalamus or somatosensory cortex markedly reduces the frequency of spike-and-wave discharges (SWDs) in the WAG/Rij model of absence epilepsy. " 07/01/2016 - "VU0360172 maintains its anti-absence effects after chronic treatment; as such, VU0360172 can also be used as a adjunctive therapy in patients with absence epilepsy. " 10/01/2014 - "Acute treatment with positive allosteric modulators (PAMs) of mGlu1 and mGlu5 metabotropic glutamate receptors (RO0711401 and VU0360172, respectively) reduces the incidence of spike-and wave discharges in the WAG/Rij rat model of absence epilepsy. "
3.	Craniocerebral Trauma (Head Injury) 10/01/2014 - "This study demonstrates that VU0360172 confers neuroprotection after experimental TBI, and suggests that mGluR5 PAMs may be promising therapeutic agents for head injury."
4.	Schizophrenia (Dementia Praecox) 01/01/2023 - "We previously demonstrated that two mGlu5 receptor-positive allosteric modulators (PAMs), VU0409551 and VU0360172, restore cognitive deficits in the sub-chronic PCP (scPCP) rodent model for schizophrenia via distinct changes in PFC intracellular signalling molecules. " 01/01/2023 - "Oscillatory Deficits in the Sub-Chronic PCP Rat Model for Schizophrenia Are Reversed by mGlu5 Receptor-Positive Allosteric Modulators VU0409551 and VU0360172." 01/01/2022 - "The comparative effects of mGlu5 receptor positive allosteric modulators VU0409551 and VU0360172 on cognitive deficits and signalling in the sub-chronic PCP rat model for schizophrenia." 01/01/2022 - "Using the sub-chronic phencyclidine rat model, widely shown to mimic the cognitive impairment and neuropathology of schizophrenia, we have investigated two mGlu5 receptor positive allosteric modulators (PAMs), VU0409551 and VU0360172. "
5.	Pain (Aches) 01/20/2016 - "Stereotaxic coadministration of VU0360172 and ACEA into the infralimbic, but not anterior cingulate, cortex mitigated decision-making deficits and pain behaviors of arthritic animals. " 01/20/2016 - "CB1-mediated depolarization-induced suppression of synaptic inhibition (DSI) was also impaired in the pain model but could be restored by coapplication of VU0360172 and ACEA. " 02/01/2014 - "A selective CB1 receptor agonist (arachidonyl-2-chloroethylamide) alone had no effect but restored the facilitatory effects of VU0360172 in the pain model. "

Related Drugs and Biologics

1.	gamma-Aminobutyric Acid (GABA)
2.	Tiagabine (Gabitril)
3.	VU0409551
4.	CB1 Cannabinoid Receptor (CB1 Receptor)
5.	Metabotropic Glutamate Receptors (Metabotropic Glutamate Receptor)
6.	Phencyclidine (Angel Dust)
7.	(3,4- dihydro- 2H- pyrano(2,3)b- quinolin- 7- yl)- (cis- 4- methoxycyclohexyl) methanone

Related Therapies and Procedures

1.	Injections
2.	Therapeutics