Stereochemistry | ABSOLUTE |
Molecular Formula | C3H7NO3 |
Molecular Weight | 105.0926 |
Optical Activity | ( + ) |
Defined Stereocenters | 1 / 1 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
N[C@H](CO)C(O)=O
InChI
InChIKey=MTCFGRXMJLQNBG-UWTATZPHSA-N
InChI=1S/C3H7NO3/c4-2(1-5)3(6)7/h2,5H,1,4H2,(H,6,7)/t2-/m1/s1
Molecular Formula | C3H7NO3 |
Molecular Weight | 105.0926 |
Charge | 0 |
Count |
MOL RATIO
1 MOL RATIO (average) |
Stereochemistry | ABSOLUTE |
Additional Stereochemistry | No |
Defined Stereocenters | 1 / 1 |
E/Z Centers | 0 |
Optical Activity | UNSPECIFIED |
SERINE, D- (D-serine) is a non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines and other amino acids. A considerable level of D-serine was discovered, surprisingly, in the mammalian brain in the early 1990s. Since then, D-serine has been considered to be a co-agonist of glutamate at the glycine site of NMDA receptors. D-serine plays an
important role in the central nervous system as an endogenous
ligand for the glycine site of glutamate N-Methyl-D-Aspartate
(NMDA) receptors. D-serine is synthetized by racemization of L-serine in most neural and non-neural cells, and modulates a variety of physiological functions in mammals. D-Serine synthesis is attributed to Serine Racemase (SR), which
catalyses the synthesis of D-serine from L-serine. D-serine may play a role in the pathophysiology
of neuropsychiatric disorders, such as schizophrenia, which may
be linked to NMDA receptor hypo-function. Studies in genetic and pharmacological animal models with decreased D-serine levels have shown that these animals displayed
behavioural abnormalities similar to those seen in schizophrenia. Moreover, exogenous administration of D-serine and related compounds improved several phenotypes relevant to schizophrenia, which could have positive clinical implications in humans. The results of a clinical trial in Taiwanese schizophrenic patients who
received D-serine as adjuvant treatment indicated that
those patients who received D-serine treatment, improved positive, negative and cognitive symptoms seen in schizophrenia. In
addition, this clinical trial showed that D-serine did not worsen
side effects from other antipsychotics, which may be due to its
selective action at the NMDA-glycine site. Therefore, D-serine
could be considered as a therapeutic approach for schizophrenia,
which is different from the dopaminergic approach. It has also been shown that exogenous d-serine administration can suppress appetite and alter food preference. Thus NMDA receptor and its co-agonist d-seine participate in the control of appetite and food preference, which can be used to suppress obesity. D-serine has been shown to have cognitive-enhancing properties in different brain disorders and in age-related cognitive decline. From a clinical perspective, it is important to highlight that in a recent double-blind placebo-controlled cross-over study our group observed that an acute oral administration of 30 mg/kg of d-serine improved spatial learning and problem solving. D-serine may be especially useful for depression because of its acute and chronic antidepressant effects,
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
---|---|---|---|
160.0 nM [EC50] |
Sample Use Guides
D-serine treatment in schizophrenia: Primary analysis was on MMN after double-blind crossover (60mg/kg/d, n=16, 6weeks) treatment with d-serine/placebo. Secondary measures included clinical symptoms, neurocognition, and the effects of open-label (30-120mg/kg/d, n=21) d-serine and bitopertin/placebo (10mg, n=29), a glycine transport inhibitor. These findings represent the first randomized double-blind placebo-controlled study with 60mg/kg d-serine in schizophrenia, and are consistent with meta-analyses showing significant effects of d-serine in schizophrenia.
Route of Administration:
Oral