Natural Nootropics Sunifiram Powder AFA CAS No. 314728-85-3 DM-235
Sunifiram (DM-235) is a synthetic derivative of Piracetam, although
due to breaking the pyrrolidone backbone it is no longer in the
Racetam class of drugs (yet by being derived from them, it is still
commonly associated with this class).
Sunifiram has mechanisms similar to Nefiracetam in the hippocampus,
and similar to that drug sunifiram shows anti-amnesiac properties
and is potentially a cognitive enhancer. Its anti-amnesiac activity
is several orders of magnitude greater than piracetam on a per
weight basis, and preliminary evidence suggest it has a similarly
low toxicity profile.
This compound is known as an AMPAkine due to exerting most of its
actions via the AMPA receptor (one of the three main subsets of
glutamate receptors, alongside NDMA and kainate). This enhancement
of AMPA function seems to also rely on enhancing signalling via the
Glycine binding site of NMDA receptors, although one minimal
signalling goes through the NMDA receptor then the benefits on AMPA
receptors seem dose-dependent.
Product Name: Sunifiram
Other Name: DM-235
CAS #: 314728-85-3
Purity: 99% min.
Molecular Formula: C14H18N2O2
Molecular Weight: 246.304
Our Sunifiram has a purity not less than 99%.
- Application Information
10-100nM of sunifiram has been noted to enhance NMDA-dependent
signalling via an increase in PKCα phosphorylation, dependent on
the glycine binding site and acting antagonistically to Glycine
(300μM). This receptor activation actiates Src, and inhibiting Src
inhibits the increase in long term potentiation. NMDA-depedent
long-term potentiation has been confirmed in vivo with 0.01-1mg/kg
oral intake of sunifiram for 7-12 days.
While signalling via the NDMA receptor exhibited a bell-curve
response peaking at 10nM it was able to cause
concentration-dependent enhancement of neuronal signalling up to
1,000nM due to an increase in AMPA receptor phosphorylation.
Increases in AMPA receptor activation was associated with an
increase in (NMDA receptor dependent) CAMKII phosphorylation and
PKCα both of which have been confirmed in vivo with 0.01-1mg/kg
sunifiram oral ingestion and are blocked by a glycine-site NMDA
antagonist. AMPA receptor activation has been noted elsewhere to be
associated with the anti-amnesiac effects of sunifiram.
Sunifiram injections at 0.01mg/kg are able to facilitate
acetylcholine release in the prefrontal cortex of rats, with no
apparent efficacy at 1mg/kg. The magnitude was around 200% of
baseline within an hour of injection.
Sunifiram is known to enhance long-term potentiation (LTP) in vitro
(10-1000nM) and in vivo (0.01-1mg/kg for 7-12 days oral intake) in
a manner that is initially dependent on the NMDA receptor
(particularly, the glycine binding site) but then positively
influences the activity of AMPA receptors.
In olfactory bulbectomized mice with hippocampal dependent memory
impairments, sunifiram at 1mg/kg is able to abolish the reductions
seen when given after training sessions. LTP in these mice
(normally impaired and causes memory dysfunction) was also
normalized to control levels.
Amnesia induced by scopolamine, baclofen, diphenhydramine, and
clonidine have all been noted to be reduced with sunifiram with
injected doses as low as 0.001mg/kg and oral doses as low as
- Reference List of Available Nootropics:
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