spec sheet11 rows
BAY 60-7550 is a potent, selective phosphodiesterase-2 (PDE2) inhibitor. By blocking PDE2 it raises both neuronal cAMP and cGMP, driving CREB phosphorylation and BDNF expression while enhancing hippocampal long-term potentiation and memory consolidation. It sits squarely in the cAMP→CREB→BDNF neighborhood but, importantly, acts on PDE2 rather than PDE4, giving it a dual second-messenger action distinct from the more familiar PDE inhibitors.
- Enhances object, social, and spatial recognition memory (rodent)
- Boosts hippocampal long-term potentiation (LTP)
- Reverses scopolamine- and MK-801-induced memory deficits (rodent)
- Aids recovery after cerebral ischemia with increased pCREB and BDNF (rodent)
- Although it lives in the same cAMP→CREB→BDNF neighborhood as PDE4 inhibitors, BAY 60-7550 targets PDE2 ; so it raises both cAMP and cGMP, a dual second-messenger action that sets it apart.
- It reliably enhances object, social, and spatial recognition memory in rodents and boosts hippocampal LTP, yet it has never been tested in humans.
- A key practical limitation is poor oral brain penetration, which restricts it to use as a laboratory probe rather than a candidate drug.
Mechanism
Selective PDE2 inhibition raises both neuronal cGMP and , enhancing and /-dependent memory consolidation. This dual second-messenger action distinguishes it from PDE4 and PDE5 inhibitors, which act through a single cyclic-nucleotide pathway.
receptor fingerprint
PDE2A (phosphodiesterase 2)Selective inhibition
cGMP / second messengersElevation of both cyclic nucleotides
Increased phosphorylation
Downstream upregulation
Evidencehow good the literature is
Preclinical only, but reproducible across independent studies: it enhances object, social, and spatial recognition memory, boosts hippocampal LTP, reverses scopolamine- and MK-801-induced deficits, and aids recovery (with increased pCREB and BDNF) after cerebral ischemia. Notably, the memory benefit appears independent of cerebrovascular effects. There is no human data.
Dosingtypical ranges, not medical advice
interested in protocols and clinical dosages? make an account to see them! ^_^
Safetyrisks and cautions, not medical advice
No human safety data exist; it is an understudied experimental probe evaluated only in animals. It should carry a cautious, investigational designation and is not suitable for human use.
History
BAY 60-7550 is a Bayer imidazotriazinone PDE2 inhibitor that became a widely used preclinical tool for probing PDE2's role in synaptic plasticity and memory. It has not entered clinical development.
Reputation
In the cognition literature BAY 60-7550 is a standard reference PDE2 inhibitor, frequently cited when researchers want to dissociate PDE2 signaling from PDE4/PDE5 effects. It has no consumer following, no human data, and its poor oral bioavailability keeps it a laboratory reagent.
Subjective profileweighing the evidence above
A preclinical-only research tool with no human data. It is a clean mechanistic probe with consistent pro-consolidation results across multiple labs, but poor oral brain penetration and the complete absence of clinical evidence mean it must be treated as strictly experimental; not a proven nootropic and not a consumer product.
Resources
This entry is here for reference.
Research
- 2004first citedInhibition of phosphodiesterase 2 increases neuronal cGMP, synaptic plasticity and memory perfo…
- 2017most recentThe phosphodiesterase type 2 inhibitor BAY 60-7550 reverses functional impairments induced by b…
- 1.Inhibition of phosphodiesterase 2 increases neuronal cGMP, synaptic plasticity and memory performance.
- 2.Phosphodiesterase inhibitors enhance object memory independent of cerebral blood flow and glucose utilization in rats.
- 3.Inhibition of phoshodiesterase type 2 or type 10 reverses object memory deficits induced by scopolamine or MK-801.
- 4.The phosphodiesterase type 2 inhibitor BAY 60-7550 reverses functional impairments induced by brain ischemia by decreasing hippocampal neurodegeneration and enhancing hippocampal neuronal plasticity.
4 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Is BAY 60-7550 a proven memory enhancer in humans?
No. All evidence is preclinical (rodent and cell models); it has never been tested in humans.
How is it different from PDE4 inhibitors?
It inhibits PDE2 rather than PDE4, so it raises both cAMP and cGMP; a dual second-messenger action, not the single-pathway effect of PDE4 or PDE5 inhibitors.
Can I take it as a nootropic?
No. There is no human dose or safety data, and poor oral brain penetration limits it to laboratory use.
Notes and cautions
- Unknown in humans (no clinical data)