Cat. No.: HY-167824

SSR180711

Name: SSR180711
Brand: MedChemExpress
SKU: HY-167824
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SSR180711 is an orally active, blood-brain barrier-penetrant α7-nAChR partial agonist (EC₅₀ = 0.9-4.4 µM; K_i = 22/14 nM for binding to rat/human α7-nAChR; IC₅₀ = 30/18 nM). SSR180711 reverses NMDA receptor antagonist-induced cognitive and latent inhibition deficits by enhancing glutamatergic and GABAergic neurotransmission, acetylcholine and Dopamine (HY-B0451) release, and long-term potentiation. SSR18071 is used in research on schizophrenia and Alzheimer's disease.

For research use only. We do not sell to patients.

Purity : 99.52%
CAS No.: 298198-52-4
Formula: C₁₄H₁₇BrN₂O₂
Molecular Weight:325.20

Storage:

Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month

SSR180711 Chemical Structure

CAS No.: 298198-52-4

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Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Purity & Documentation
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target

^[7]^[4]

α7-nAChR

22 nM (Ki, rat)

α7-nAChR

14.71 nM (Ki, human)

α7-nAChR

30 nM (IC₅₀, rat)

α7-nAChR

18 nM (IC₅₀, human)

α7-nAChR

4.4 μM (EC₅₀, Xenopus oocytes)

α7-nAChR

0.9 μM (EC₅₀, GH4C1 cells)

All Endogenous Metabolite Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
GH4-C1	EC50	0.9 μM	Agonist activity at recombinant human α7 nAChRs expressed in GH4C1 cells assessed by whole-cell patch-clamp at -60 mV; partial agonist with intrinsic activity 36% versus 1 mM ACh. Agonist activity at recombinant human α7 nAChRs expressed in GH4C1 cells assessed by whole-cell patch-clamp at -60 mV; partial agonist with intrinsic activity 36% versus 1 mM ACh.	17019409

In Vitro

Glutamate Release or ReceptorsOthers

Glutamate Release or Receptors

SSR180711 (0.3-1 µM for EPSCs; 0.03-0.1 µM for IPSCs) increases glutamatergic EPSCs and GABAergic IPSCs in mouse CA1 hippocampal slices through α7 nAChR activation, with the maximum effect on EPSCs at 0.3-1 µM and the maximum effect on IPSCs at 0.03-0.1 µM^[4].
SSR180711 (300 nM) enhances LTP in rat and mouse CA1 hippocampal slices through α7 nAChR activation^[4].

Others

SSR180711 (10^-10-10^-6 M; preincubated at 37°C for 30 minutes, followed by incubation with radioligand for 60 minutes) binds with high affinity to rat and human α7 nAChRs (IC₅₀ of 30 and 18 nM, respectively) and is selective for hα4β2, hα3β2, hα3β4, and hα1β1γδ nAChRs^[4].
SSR180711 (4.4 µM) is a partial agonist of human α7 nAChRs expressed in Xenopus oocytes, with an EC₅₀ of 4.4 µM and an intrinsic activity of 51% of the ACh response^[4].
SSR180711 (0.9 µM) is a partial agonist of human α7 nAChRs expressed in GH4C1 cells, with an EC₅₀ of 0.9 µM and an intrinsic activity of 36%^[4].
SSR180711 (100 µM) does not activate hα1β1γδ, hα3β2, or hα3β4 nAChRs^[4].
SSR180711 (1 µM) activates native rat hippocampal α7 nAChRs at presynaptic and somatodendritic locations^[4].
SSR180711 (14-22 nM) binds to α7 nAChR with a K_i of 22 nM in rat receptors and a K_i of 14 nM in human receptors^[7].
SSR180711 (10 μM; 2 minutes), when co-applied with PNU 120596 (HY-12152) (3 μM), increases sIPSC frequency to a lesser extent in PFC layer II/III pyramidal neurons of subchronically SSR180711-exposed rats than in control rats^[9].
SSR180711 does not reverse the increase in THIP (HY-10232)-induced currents in rat PFC layer II/III pyramidal neurons induced by early postnatal challenge after subchronic exposure^[9].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Parmacokinetics

Species	Dose	Route	Brain Concentration	T_1/2
Mice^[9]	3 mg/kg	s.c.	approximately 5000 ng/g	approximately 1 h

In Vivo

Glutamate Release or ReceptorsOxidative StressOthers

Glutamate Release or Receptors

SSR180711 (0.1-1 mg/kg; intravenous injection; single bolus) dose-dependently increases the firing frequency of ventral pallidum neurons in anesthetized Sprague-Dawley rats, and this effect is blocked by Methyllycaconitine (MLA) (HY-N2332) and reversed by Dizocilpine (MK-801) (HY-15084B)^[4].
SSR180711 (0.3-3 mg/kg; i.p.; administered 30 minutes before exposure and 30 minutes before conditioning) reverses MK801-induced persistent latent inhibition at doses of 1 and 3 mg/kg, but has no such effect at 0.3 mg/kg^[7].

Oxidative Stress

SSR180711 (0.3-3 mg/kg; i.p.; administered 30 minutes before exposure and 30 minutes before conditioning) reverses persistent latent inhibition induced by neonatal NG-nitro-L-arginine (L-NoArg) (HY-12115)^[7].

Others

SSR180711 (0.5-5 mg/kg; intravenous bolus; single dose; 90 min before ¹⁸F-ASEM injection) produces dose-dependent blockade of ¹⁸F-ASEM binding in baboon brain, with mean α7-nAChR occupancy increasing from 38% at 0.5 mg/kg to 80.5% at 5 mg/kg^[1].
SSR180711 (0.1-30.0 mg/kg; subcutaneous injection; 5 minutes before testing) does not improve probabilistic reversal learning ability in normal C57BL/6 mice^[2].
SSR180711 (3 mg/kg; intravenous injection via the lateral tail vein; acute single administration) reduces spontaneously active VTA DA neurons in MAM rats, and this reduction is most pronounced in the lateral VTA^[3].
SSR180711 (5.0 μg; bilateral intracerebral infusion into the vHipp; acute administration; infused slowly at 0.25 µL/min for 2 minutes, with the first 15 minutes recorded) restores the population activity and firing rate of VTA DA neurons in MAM rats to normal; it increases the population activity of VTA DA neurons in control rats, especially in the central region of the VTA^[3].
SSR180711 (5.0 μg; bilateral intracerebral infusion into the BLA; acute administration; infused slowly at 0.25 µL/min for 2 minutes, with recording during the first 15 minutes) does not alter the elevated population activity of VTA DA neurons in MAM rats, but increases burst firing of VTA DA neurons^[3].
SSR180711 (3-30 mg/kg; intraperitoneal or oral administration; single dose) increases extracellular ACh levels in the hippocampus and prefrontal cortex of freely moving Sprague-Dawley rats^[4].
SSR180711 (0.3-3.0 mg/kg; intraperitoneal injection; single administration; day 15) does not improve NMDA receptor antagonist-induced cognitive deficits in mice^[5].
SSR180711 (3.0 mg/kg/day; intraperitoneal injection; once daily; days 15-28) ameliorates NMDA receptor antagonist-induced cognitive deficits in mice but does not reverse NMDA receptor antagonist-induced reduction of α7 nAChR, and this cognitive effect is blocked by MLA^[5].
SSR180711 (0.3-10 mg/kg; oral; 60 minutes before each of three tests) enhances long-term episodic memory in healthy rats and maintains efficacy after repeated administration^[6].
SSR180711 (0.1-3 mg/kg; oral; 60 minutes before each of three tests) improves long-term recognition memory in C57Bl/6j mice^[6].
SSR180711 (0.3 mg/kg; intraperitoneal injection) improves long-term object recognition in wild-type mice but not in α7 nAChR knockout mice^[6].
SSR180711 (0.3-1 mg/kg; oral; in combination with MK-801) reverses MK-801-induced short-term episodic memory deficits in rats^[6].
SSR180711 (3-10 mg/kg; intraperitoneal injection; 30 minutes before each training day) attenuates MK-801-induced working memory deficits in rats^[6].
SSR180711 (1 mg/kg; oral; administered immediately after acquisition training) reverses visual memory deficits induced by NMDA receptor antagonist sensitization in rats^[6].
SSR180711 (maximum dose 1 mg/kg; oral; 60 minutes before exposure to the first pup) reverses neonatal NMDA receptor antagonist-induced selective attention deficits in adult rats^[6].
SSR180711 (1-3 mg/kg; oral or intraperitoneal injection; 45 minutes before daily learning training) partially reverses NMDA receptor antagonist-induced sequential memory deficits in rats^[6].
SSR180711 (1-3 mg/kg; intravenous injection; within 1 minute) increases the spontaneous firing of neurons in the rat retrosplenial cortex^[6].
SSR180711 (1 mg/kg; intraperitoneal injection) increases extracellular Dopamine (HY-B0451) levels in the rat prefrontal cortex^[6].
SSR180711 (1-10 mg/kg; p.o.; administered 15 minutes before testing and 60 minutes before testing) reduces immobility time in the rat forced swim test^[6].
SSR180711 (1-10 mg/kg; s.c.) reduces maternal separation-induced ultrasonic distress vocalizations in rat pups^[6].
SSR180711 (10 mg/kg; i.p.; once daily for 22 days) attenuates chronic mild stress-induced fur deterioration in mice^[6].
SSR180711 (1-3 mg/kg; i.p.; administered 30 minutes before exposure and 30 minutes before conditioning) reverses psychostimulant-induced disruption of latent inhibition at doses of 1 and 3 mg/kg^[7].
SSR180711 (0.3-3 mg/kg; i.p.; administered 30 minutes before exposure and 30 minutes before conditioning) enhances latent inhibition in healthy rats at doses of 1 and 3 mg/kg under strong conditioning, but has no such effect at a dose of 0.3 mg/kg^[7].
SSR180711 (0.3-3 mg/kg; i.p.; administered 30 minutes before exposure and 30 minutes before conditioning) enhances latent inhibition in neonatally vehicle-treated rats at doses of 1 and 3 mg/kg under strong conditioning, but has no such effect at a dose of 0.3 mg/kg^[7].
SSR180711 (1-3 mg/kg; i.p.; administered 30 minutes before exposure and 30 minutes before conditioning) does not disrupt latent inhibition in healthy rats under weak conditioning^[7].
SSR180711 (3-20 mg/kg; s.c.; single injection; 2 hours) dose-dependently induces c-Fos in the ACCshell and PFC of rats, but not in the ACCcore or STRdl, and this induction is blocked by MLA^[8].
SSR180711 induces c-Fos in the ACCshell and mPFC of wild-type mice, but not in α7 nAChR knockout mice^[8].
SSR180711 (3 mg/kg; s.c.; twice daily; for 7 days) reverses early postnatal NMDA antagonist-induced prepulse inhibition deficits of startle reflex in adolescent Lister hooded rats^[9].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

C57BL/6NJ (male; also referred to as C57BL/6J; 3 months old; 23-30 g at start of training)^[2]
Dosage:

0.1, 0.3, 1.0, 3.0, 10.0, and 30.0 mg/kg; first session 3.0, 10.0, or 30.0 mg/kg; 14 days later 0.1, 0.3, or 1.0 mg/kg
Administration:

s.c.; two PRLT test sessions 14 days apart; 5 min prior to testing
Result:

Dprime values in the PRLT were -0.01 at 3.0 mg/kg, -0.21 at 10.0 mg/kg, 0.02 at 30.0 mg/kg, 0.23 at 0.1 mg/kg, 0.21 at 0.3 mg/kg, and 0.21 at 1.0 mg/kg.
No effect was observed on total trials to criterion or number of reversals at either high-dose (3.0, 10.0, 30.0 mg/kg) or lower-dose (0.1, 0.3, 1.0 mg/kg) sessions.
Initial or reversal learning in the PRLT was not improved.

Animal Model:

Sprague-Dawley (male, adult PND65-140, offspring of MAM-treated dams)^[3]
Dosage:

3 mg/kg (calculated as free base)
Administration:

i.v. via lateral tail vein; acute single administration
Result:

In MAM rats, VTA DA neuron population activity reduced to 1.0 cells/track.
In the lateral VTA of MAM rats, population activity reduced to 0.8 cells/track versus 1.9 cells/track in the MAM + vehicle group.

Animal Model:

Sprague-Dawley (male, adult PND65-140, offspring of MAM-treated dams)^[3]
Dosage:

5.0 μg (calculated as free base)
Administration:

bilateral intracerebral infusion into vHipp; acute administration; slow infusion at 0.25 µL/min for 2 min, 15 min before recording
Result:

In MAM rats, VTA DA neuron population activity reduced to 1.0 cells/track.
In the lateral VTA of MAM rats, population activity reduced to 0.6 cells/track versus 1.7 cells/track in the MAM + vehicle group.
The elevated MAM DA neuron average firing rate reversed to 3.1 Hz.

Animal Model:

Sprague-Dawley (male, adult PND65-140, offspring of saline-treated dams)^[3]
Dosage:

5.0 μg (calculated as free base)
Administration:

bilateral intracerebral infusion into BLA; acute administration; slow infusion at 0.25 µL/min for 2 min, 15 min before recording
Result:

In control rats, VTA DA neuron population activity increased to 1.6 cells/track.
In the central VTA of control rats, population activity increased to 1.8 cells/track versus 0.7 cells/track in controls.

Animal Model:

Sprague-Dawley (male, adult PND65-140, offspring of MAM-treated dams)^[3]
Dosage:

5.0 μg (calculated as free base)
Administration:

bilateral intracerebral infusion into BLA; acute administration; slow infusion at 0.25 µL/min for 2 min, 15 min before recording
Result:

In MAM rats, VTA DA neuron population activity was not altered.
MAM rats showed elevated VTA DA neuron population activity (1.6 cells/track) that was not significantly changed versus vehicle.
Burst firing of 30.5% of spikes in VTA DA neurons was produced versus 18.5% for the MAM + vehicle group.

Animal Model:

Sprague-Dawley (male, 280-400 g)^[4]
Dosage:

0.1 mg/kg i.v.; 0.3 mg/kg i.v.; 1 mg/kg i.v.; single i.v. bolus
Administration:

i.v.; single bolus
Result:

Dose-dependently increased the firing rate of VP neurons after i.v. administration at 0.1 mg/kg (n=4), 0.3 mg/kg (n=5), and 1 mg/kg (n=7).
At 1 mg/kg i.v., the effect was seen from the first 5 min (+196% with respect to baseline) and reached +339% 30 min after administration.
All recorded cells were activated by 0.3 and 1 mg/kg i.v. (n=5 and n=7, respectively).
MLA (0.3 mg/kg i.v.) administered 30 min after the 1 mg/kg i.v. injection completely blocked the enhancing effect, with a maximum fall of 92.5% at 15 min relative to the pre-MLA level.
MK-801 (0.03 mg/kg i.v.) administered 15 min after the 1 mg/kg i.v. injection fully reversed the increase, with a maximum drop of 88.8% at 10 min after MK-801 administration.

Animal Model:

Sprague-Dawley (adult male, 250-330 g)^[4]
Dosage:

10 mg/kg i.p.; 3 mg/kg i.p.; 30 mg/kg p.o.; 10 mg/kg p.o.; single i.p. or p.o. administration
Administration:

i.p. or p.o.; single administration
Result:

Produced dose-dependent increases in ACh release.
Maximal increases were 190% at 40 min for 10 mg/kg i.p. in the hippocampus and 176% of basal value at 60 min for 3 mg/kg i.p. in the prefrontal cortex.

Animal Model:

ICR (male, 6 weeks old, 25-30 g)^[5]
Dosage:

0.3 or 3.0 mg/kg
Administration:

i.p.; single administration; day 15
Result:

Repeated NMDA receptor antagonist administration reduced exploratory preference to approximately 40% compared with approximately 50% in saline control mice.
Did not alter the reduction of exploratory preference in mice with repeated NMDA receptor antagonist administration at 0.3 or 3.0 mg/kg.
In the training session, there were no differences among groups in total exploration time or exploratory preference.

Animal Model:

ICR (male, 6 weeks old, 25-30 g)^[5]
Dosage:

0.3 mg/kg/day; 3.0 mg/kg/day; 3.0 mg/kg/day (with MLA 3.0 mg/kg/day)
Administration:

i.p.; once daily; days 15-28
Result:

In the NORT training session, exploratory preferences among groups were not different.
In the retention session, 3.0 mg/kg/day improved NMDA receptor antagonist-induced cognitive deficits, whereas 0.3 mg/kg/day did not.
Co-administration of MLA (3.0 mg/kg/day) antagonized the improvement at 3.0 mg/kg/day.
Did not alter the reduction of α7 nAChRs in the frontal cortex or hippocampus after repeated NMDA receptor antagonist administration at 3.0 mg/kg/day.

Animal Model:

C57Bl/6j (male, 10-week old, 17-32 g)^[6]
Dosage:

0.1-3 mg/kg p.o.
Administration:

p.o.; 60 min before each of three sessions
Result:

Increased the time spent investigating the novel object from 0.3 mg/kg.
Differed from chance level (0.5) from 0.3 mg/kg, with effects at 0.3, 1, and 3 mg/kg.

Animal Model:

C57Bl/6j (male, α7 nAChR knockout and wild-type littermates, 20-32 weeks old, 32-35 g)^[6]
Dosage:

0.3 mg/kg i.p.
Administration:

i.p.; single dose
Result:

At the 48-h retention delay, 0.3 mg/kg i.p. improved the amount of time spent investigating the novel object in WT mice but not in α7 nAChR KO mice.

Animal Model:

Sprague-Dawley or Wistar (male, 180-350 g)^[6]
Dosage:

0.3 and 1 mg/kg p.o. with MK-801; separate: 0.3 mg/kg i.p. with MK-801 and MLA 3 mg/kg i.p.
Administration:

p.o.; with MK-801; separate: i.p. with MK-801 and MLA 3 mg/kg i.p.
Result:

0.3 and 1 mg/kg p.o. restored preferential investigation of the novel object in rats given MK-801.
0.3 mg/kg i.p. restored the deficit; coadministered MLA abolished this effect.

Animal Model:

Wistar (male, 250-300 g at start of study)^[6]
Dosage:

3 and 10 mg/kg i.p.
Administration:

i.p.; 30 min before each training day
Result:

Mean overall times to reach the platform were 80.34 s for 3 mg/kg i.p. and 73.76 s for 10 mg/kg i.p.

Animal Model:

Sprague-Dawley or Wistar (male)^[6]
Dosage:

1 mg/kg p.o.
Administration:

p.o.; immediately after acquisition session
Result:

1 mg/kg p.o. reversed the effects of an acute challenge with an NMDA receptor antagonist 1 mg/kg i.p. in rats given an NMDA receptor antagonist repeatedly.

Animal Model:

Wistar Han (male, neonatally treated, tested as adults between PN 118 and PN 142)^[6]
Dosage:

p.o. four doses, highest reported dose 1 mg/kg; separate: 3 mg/kg i.p. followed by MLA 3 mg/kg s.c.
Administration:

p.o.; 60 min before exposure to first juvenile; separate: i.p. followed by MLA 3 mg/kg s.c.
Result:

Dose-dependently normalized the novelty discrimination impairment; a difference was reported at the highest dose of 1 mg/kg.
In vehicle-neonatal control rats, had no effect by itself.

Animal Model:

Sprague-Dawley or Wistar (male, N=20 per group)^[6]
Dosage:

1 and 3 mg/kg (p.o. per Methods; i.p. per Results)
Administration:

p.o. (Methods) or i.p. (Results); 45 min before each daily learning session
Result:

1 and 3 mg/kg partially diminished the number of errors induced by an NMDA receptor antagonist across all five learning sessions.
When errors were cumulated across all five sessions, both doses lowered the error rate relative to the NMDA receptor antagonist-injected group.

Animal Model:

Sprague-Dawley or Wistar (male, N=3-6 per group)^[6]
Dosage:

1 and 3 mg/kg i.v.; separate: 3 mg/kg i.v. after MLA 1 mg/kg i.v.
Administration:

i.v.; over 1 min; separate: i.v. after MLA 1 mg/kg i.v.
Result:

1 mg/kg i.v. produced a small 19% decrease at a single time point (10 min).
At 3 mg/kg i.v., doubled the firing rate, with effects observed from 5 to 20 min post-administration.
MLA fully reversed the increase produced by 3 mg/kg.

Animal Model:

Sprague-Dawley or Wistar (male, N=7-9 per group)^[6]
Dosage:

1 mg/kg i.p.; separate: 1 mg/kg i.p. after MLA 3 mg/kg i.p.
Administration:

i.p.; separate: i.p. after MLA 3 mg/kg i.p.
Result:

The average basal extracellular dopamine level was 7.6 fmol per fraction.
1 mg/kg i.p. increased extracellular dopamine levels, with a maximal effect of 164% of basal value at 20 min.
MLA completely prevented the increase induced by 1 mg/kg.

Animal Model:

Sprague-Dawley or Wistar (male, N=7-8 per group)^[6]
Dosage:

1, 3, and 10 mg/kg p.o.
Administration:

p.o.; 15 min after pre-test and 60 min before test
Result:

Time spent in immobility was 170.9 s at 1 mg/kg, 150.4 s at 3 mg/kg, and 114.9 s at 10 mg/kg.

Animal Model:

BALB/c (male, 6-week old, 17-32 g)^[6]
Dosage:

10 mg/kg i.p. once daily for 22 days
Administration:

i.p.; once daily for 22 days
Result:

Attenuated stress-induced degradation of the physical state of the coat at day 29 and day 36.
At the end of the stress period, the stressed group reached the level of nonstressed controls.

Animal Model:

Wistar (male; 350-510 g; adult)^[7]
Dosage:

0.3 mg/kg; 1 mg/kg; 3 mg/kg
Administration:

i.p.; 30 min before pre-exposure and 30 min before conditioning
Result:

In MK801-treated rats, persistent LI was present in the vehicle and 0.3 mg/kg groups.
At 1 mg/kg and 3 mg/kg, MK801-induced persistent LI was reversed; PE and NPE groups did not differ.

Animal Model:

Wistar (male; neonatal L-NoArg exposure; tested as adults at 3 months of age)^[7]
Dosage:

0.3 mg/kg; 1 mg/kg; 3 mg/kg
Administration:

i.p.; 30 min before pre-exposure and 30 min before conditioning
Result:

In neonatal L-NoArg rats, persistent LI was present with vehicle.
At 0.3-3 mg/kg, persistent LI was reversed; PE and NPE groups did not differ.

Animal Model:

Wistar (male; 350-510 g; adult)^[7]
Dosage:

1 mg/kg; 3 mg/kg
Administration:

i.p.; 30 min before pre-exposure and 30 min before conditioning
Result:

In psychostimulant-treated rats, LI was disrupted with vehicle.
At 1-3 mg/kg, psychostimulant-induced LI disruption was reversed; PE and NPE groups showed LI.

Animal Model:

Wistar (male; 350-510 g; adult)^[7]
Dosage:

0.3 mg/kg; 1 mg/kg; 3 mg/kg
Administration:

i.p.; 30 min before pre-exposure and 30 min before conditioning
Result:

In vehicle-treated rats, LI was absent with vehicle and 0.3 mg/kg.
At 1-3 mg/kg, LI was potentiated with strong conditioning; PE and NPE groups showed LI.

Animal Model:

Wistar (male; neonatal vehicle exposure; tested as adults at 3 months of age)^[7]
Dosage:

0.3 mg/kg; 1 mg/kg; 3 mg/kg
Administration:

i.p.; 30 min before pre-exposure and 30 min before conditioning
Result:

In neonatally vehicle-treated rats, LI was absent with vehicle and 0.3 mg/kg.
At 1-3 mg/kg, LI was potentiated; PE and NPE groups showed LI.

Animal Model:

Wistar (male; 350-510 g; adult)^[7]
Dosage:

1 mg/kg; 3 mg/kg
Administration:

i.p.; 30 min before pre-exposure and 30 min before conditioning
Result:

In vehicle-treated rats, LI was present with vehicle and at 1-3 mg/kg; PE and NPE groups showed LI.

Animal Model:

Wistar (adult male, 250-300 g; Taconic Europe)^[8]
Dosage:

3, 10, or 20 mg/kg; 10 mg/kg (after MLA 10 mg/kg)
Administration:

s.c.; single injection; 2 hr
Result:

Induced a dose-dependent increase in c-Fos expression in the ACCshell; some c-Fos immunostaining was observed at 3 mg/kg, and the number of c-Fos-positive neurons increased about three-fold at 10 mg/kg and 20 mg/kg.
In PFC subdivisions, about a three-fold induction was observed in mPFC, CCTX, and ILCTX.
The effect was dose-dependent, with the lowest effective dose at 3 mg/kg and a plateau at 10 mg/kg.
Did not affect basal c-Fos levels in the ACCcore or STRdl at any dose tested.
Pre-administration of MLA effectively inhibited c-Fos expression in ACCshell and mPFC; MLA alone had no effect on c-Fos expression.

Animal Model:

Lister hooded (adolescent, PND 33-36 at testing; 79 g model group, 93 g vehicle group at testing)^[9]
Dosage:

3 mg/kg
Administration:

s.c.; twice daily (7-8 am and 7-8 pm); for 7 days; initiated PND 25-28; 36-h washout before testing on PND 33-36
Result:

Reversed the early postnatal NMDA antagonist-induced PPI deficit in the subset.
A significant early postnatal × subchronic interaction was present (F(1,27)=7.04).
The early postnatal NMDA antagonist-induced PPI reduction was evident in saline-exposed model animals and was ameliorated.
Significantly increased ASR (F(1,28)=7.63), affecting both early postnatal saline and model animals.
An early postnatal × subchronic interaction for ITA (F(1,28)=4.24) indicated that ITA was affected differently in vehicle and model animals.
Group sizes for PPI were vehicle n=8 and model n=8.

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Chemical Information

CAS No. 298198-52-4
Appearance Solid
Molecular Weight 325.20
Formula C₁₄H₁₇BrN₂O₂
Color Off-white to light brown
SMILES

O=C(N1CCN2CCC1CC2)OC3=CC=C(C=C3)Br
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
In solvent	-80°C	6 months
	-20°C	1 month

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (317 KB)
SDS (644 KB)
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COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
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IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Horti AG, et al. 18F-ASEM, a radiolabeled antagonist for imaging the α7-nicotinic acetylcholine receptor with PET. Journal of nuclear medicine : official publication, Society of Nuclear Medicine. 2014 Apr;55(4):672-7.

[2]. Milienne-Petiot M, et al. Nicotine improves probabilistic reward learning in wildtype but not alpha7 nAChR null mutants, yet alpha7 nAChR agonists do not improve probabilistic learning. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology. 2018 Nov;28(11):1217-1231.

[3]. Neves GA, et al. α7 Nicotinic receptor-modulating agents reverse the hyperdopaminergic tone in the MAM model of schizophrenia. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2018 Jul;43(8):1712-1720.

[4]. Biton B, et al. SSR180711, a novel selective alpha7 nicotinic receptor partial agonist: (1) binding and functional profile. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2007 Jan;32(1):1-16. [Content Brief]

[5]. Hashimoto K, et al. Phencyclidine-induced cognitive deficits in mice are improved by subsequent subchronic administration of the novel selective alpha7 nicotinic receptor agonist SSR180711. Biological psychiatry. 2008 Jan 01;63(1):92-7.

[6]. Pichat P, et al. SSR180711, a novel selective alpha7 nicotinic receptor partial agonist: (II) efficacy in experimental models predictive of activity against cognitive symptoms of schizophrenia. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2007 Jan;32(1):17-34.

[7]. Barak S, et al. Pro-cognitive and antipsychotic efficacy of the alpha7 nicotinic partial agonist SSR180711 in pharmacological and neurodevelopmental latent inhibition models of schizophrenia. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2009 Jun;34(7):1753-63.

[8]. Hansen HH, et al. Alpha-7 nicotinic acetylcholine receptor agonists selectively activate limbic regions of the rat forebrain: an effect similar to antipsychotics. Journal of neuroscience research. 2007 Jun;85(8):1810-8.

[9]. Kjaerby C, et al. Repeated potentiation of the metabotropic glutamate receptor 5 and the alpha 7 nicotinic acetylcholine receptor modulates behavioural and GABAergic deficits induced by early postnatal phencyclidine (PCP) treatment. Neuropharmacology. 2013 Sep;72:157-68.

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SSR180711

All Endogenous Metabolite Isoforms