spec sheet11 rows
Tulrampator (S-47445) is a selective positive allosteric modulator of AMPA-type glutamate receptors developed by Servier. Beyond acutely potentiating glutamatergic transmission, it upregulates BDNF and NT-3, activates the mTOR/CREB plasticity pathway, and rescues age-related deficits in hippocampal long-term potentiation and synaptic architecture in animals. It is the best-characterized modern AMPA-PAM and the only ampakine of its cohort to reach large Phase 2 human trials.
- Selective AMPA-receptor positive allosteric modulation
- Upregulates BDNF, NT-3 and NGF in preclinical models
- Rescues age-impaired hippocampal LTP and dendritic spine density
- Shows memory synergy with donepezil in aged-mouse models
- Nausea (reported in Phase 2 trials)
- Dizziness
- Headache
- Long-term and consumer safety unknown
- Tulrampator is the only ampakine in its cohort to reach large Phase 2 human trials.
- It raises BDNF, NT-3 and NGF, making it a rare small molecule that bridges AMPA potentiation to the neurotrophic cascade.
- Despite excellent preclinical data, its Alzheimer's Phase 2 in roughly 520 patients showed no ADAS-Cog benefit over placebo.
Mechanism
-receptor positive modulator that slows receptor deactivation and desensitization (EC50 ~2.5-5.4 uM across GluA1/2/4 flip/flop variants), enhancing fast excitatory transmission and . Downstream it drives phosphorylation, upregulates /NT-3/, and engages /4E-BP1 signaling, restoring boutons and dendritic spines. It is also neuroprotective against in vitro.
receptor fingerprint
receptors (GluA1-4)Positive allosteric modulation
/ signalingUpregulation (downstream)
Phosphorylation / activation
NT-3 / Upregulation
/ 4E-BP1Pathway activation
Evidencehow good the literature is
Robust preclinical support from multiple independent labs, but negative human Phase 2 data. The Alzheimer's Phase 2 (NCT02626572, ~520 patients, 24 weeks, 5/15/50 mg) showed no significant ADAS-Cog benefit versus placebo (largest difference -0.90, p=0.29; Bernard et al. 2019). An adjunctive major-depression Phase 2 (NCT02805439, ~400 patients) completed without demonstrating superiority to placebo. Preclinically it rescues age-impaired CA3-CA1 LTP, restores VGlut1+ boutons and dendritic spines, corrects age-related BDNF/NT-3/NGF deficits, shows synergy with donepezil, and produces antidepressant/anxiolytic-like effects via neurogenesis-dependent and -independent routes.
Dosingtypical ranges, not medical advice
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Safetyrisks and cautions, not medical advice
In rodents, no convulsions or tremor up to 1000 mg/kg acute. In human Phase 2 trials the reported adverse events were nausea, dizziness, and headache. Human safety was characterized only over the trial durations; long-term and consumer safety are unknown, and it is not available as a supplement.
History
Developed by Servier as S-47445 (also designated CX-1632). It advanced to two large Phase 2 programs: an Alzheimer's disease trial (NCT02626572) and an adjunctive major-depressive-disorder trial (NCT02805439). Both failed to demonstrate superiority to placebo (Bernard et al. 2019 reported the negative Alzheimer's primary endpoint), and development did not advance further.
Reputation
Within nootropic and neuroscience circles it is regarded as the most modern, best-characterized AMPA-PAM with an explicit BDNF/CREB/mTOR story, often cited as the cleanest small-molecule bridge from AMPA potentiation to the neurotrophic cascade. Informed commentators emphasize that despite this, its human Phase 2 results were negative and it is not obtainable as a product.
Subjective profileweighing the evidence above
Mechanistically the most complete AMPA-PAM story available, cleanly bridging AMPA potentiation to the BDNF/CREB/mTOR neurotrophic cascade in preclinical models. However, its two Phase 2 human trials (Alzheimer's disease and adjunctive major depression) failed to beat placebo, and it is not a marketed or grey-market product. Treat it as an investigational compound with strong mechanism but no demonstrated human cognitive benefit.
Resources
This entry is here for reference.
Research
- 1.Pharmacological characterisation of S 47445, a novel positive allosteric modulator of AMPA receptors.
- 2.The AMPA receptor positive allosteric modulator S 47445 rescues in vivo CA3-CA1 long-term potentiation and structural synaptic changes in old mice.
- 3.Upregulation of neurotrophins by S 47445, a novel positive allosteric modulator of AMPA receptors in aged rats.
- 4.Synergistic enhancing-memory effect of donepezil and S 47445, an AMPA positive allosteric modulator, in middle-aged and aged mice.
- 5.S 47445 Produces Antidepressant- and Anxiolytic-Like Effects through Neurogenesis Dependent and Independent Mechanisms.
5 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Is Tulrampator an approved cognitive enhancer?
No. It is an investigational AMPA-PAM. Its two Phase 2 trials (Alzheimer's disease and adjunctive major depression) failed to beat placebo, and it is not marketed or sold as a supplement.
What makes it mechanistically interesting?
It is the cleanest small-molecule bridge from AMPA-receptor potentiation to the BDNF/CREB/mTOR neurotrophic cascade, restoring LTP and synaptic architecture in aged animals.
Can I buy it?
No. There is no consumer or grey-market product and no established nootropic dosing standard.
Adverse effects
- Nausea (reported in Phase 2 trials)
- Dizziness
- Headache
- Long-term and consumer safety unknown