<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">4372</id>
  <title>T3D4318</title>
  <common-name>Glycine</common-name>
  <description>Glycine is a simple, nonessential amino acid, although experimental animals show reduced growth on low-glycine diets. The average adult ingests 3 to 5 grams of glycine daily. Glycine is involved in the body's production of DNA, phospholipids and collagen, and in release of energy. Glycine levels are effectively measured in plasma in both normal patients and those with inborn errors of glycine metabolism. Nonketotic hyperglycinaemia (OMIM 606899) is an autosomal recessive condition caused by deficient enzyme activity of the glycine cleavage enzyme system (EC 2.1.1.10). The glycine cleavage enzyme system comprises four proteins: P-, T-, H- and L-proteins (EC 1.4.4.2, EC 2.1.2.10 and EC 1.8.1.4 for P-, T- and L-proteins). Mutations have been described in the GLDC (OMIM 238300), AMT (OMIM 238310), and GCSH (OMIM 238330) genes encoding the P-, T-, and H-proteins respectively. The glycine cleavage system catalyses the oxidative conversion of glycine into carbon dioxide and ammonia, with the remaining one-carbon unit transferred to folate as methylenetetrahydrofolate. It is the main catabolic pathway for glycine and it also contributes to one-carbon metabolism. Patients with a deficiency of this enzyme system have increased glycine in plasma, urine and cerebrospinal fluid (CSF) with an increased CSF: plasma glycine ratio.  (A3412). t is also a fast inhibitory neurotransmitter.</description>
  <cas>56-40-6</cas>
  <pubchem-id>750</pubchem-id>
  <chemical-formula>C2H5NO2</chemical-formula>
  <weight>75.07</weight>
  <appearance>White powder.</appearance>
  <melting-point>262 dec°C</melting-point>
  <boiling-point></boiling-point>
  <density nil="true"/>
  <solubility>2.49E+005 mg/L (at 25°C)</solubility>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Absorbed from the small intestine via an active transport mechanism.</route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>In the CNS, there exist strychnine-sensitive glycine binding sites as well as strychnine-insensitive glycine binding sites. The strychnine-insensitive glycine-binding site is located on the NMDA receptor complex. The strychnine-sensitive glycine receptor complex is comprised of a chloride channel and is a member of the ligand-gated ion channel superfamily. The putative antispastic activity of supplemental glycine could be mediated by glycine's binding to strychnine-sensitive binding sites in the spinal cord. This would result in increased chloride conductance and consequent enhancement of inhibitory neurotransmission. The ability of glycine to potentiate NMDA receptor-mediated neurotransmission raised the possibility of its use in the management of neuroleptic-resistant negative symptoms in schizophrenia. &lt;br/&gt;Animal studies indicate that supplemental glycine protects against endotoxin-induced lethality, hypoxia-reperfusion injury after liver transplantation, and D-galactosamine-mediated liver injury. Neutrophils are thought to participate in these pathologic processes via invasion of tissue and releasing such reactive oxygen species as superoxide. In vitro studies have shown that neutrophils contain a glycine-gated chloride channel that can attenuate increases in intracellular calcium and diminsh neutrophil oxidant production. This research is ealy-stage, but suggests that supplementary glycine may turn out to be useful in processes where neutrophil infiltration contributes to toxicity, such as ARDS.</mechanism-of-toxicity>
  <metabolism>Hepatic</metabolism>
  <toxicity>ORL-RAT LD&lt;sub&gt;50&lt;/sub&gt; 7930 mg/kg, SCU-RAT LD&lt;sub&gt;50&lt;/sub&gt; 5200 mg/kg, IVN-RAT LD&lt;sub&gt;50&lt;/sub&gt; 2600 mg/kg, ORL-MUS LD&lt;sub&gt;50&lt;/sub&gt; 4920 mg/kg</toxicity>
  <lethaldose nil="true"/>
  <carcinogenicity>No indication of carcinogenicity to humans (not listed by IARC).</carcinogenicity>
  <use-source>Supplemental glycine may have antispastic activity. Very early findings suggest it may also have antipsychotic activity as well as antioxidant and anti-inflammatory activities.</use-source>
  <min-risk-level nil="true"/>
  <health-effects>Chronically high levels of glycine are associated with at least 12 inborn errors of metabolism including: Citrullinemia Type I, Hyperglycinemia, non-ketotic, Hyperprolinemia Type I, Hyperprolinemia Type II, Iminoglycinuria, Isovaleric Aciduria, Malonic Aciduria, Methylmalonic Aciduria, Methylmalonic Aciduria Due to Cobalamin-Related Disorders, Non Ketotic Hyperglycinemeia, Prolinemia Type II, Propionic academia and Short Chain Acyl CoA Dehydrogenase Deficiency (SCAD Deficiency).</health-effects>
  <symptoms nil="true"/>
  <treatment nil="true"/>
  <created-at type="dateTime">2014-08-29T06:21:32Z</created-at>
  <updated-at type="dateTime">2026-05-14T16:24:16Z</updated-at>
  <interacting-proteins nil="true"/>
  <wikipedia>Glycine</wikipedia>
  <uniprot-id nil="true"/>
  <kegg-compound-id>C00037</kegg-compound-id>
  <omim-id nil="true"/>
  <chebi-id>15428</chebi-id>
  <biocyc-id>GLY</biocyc-id>
  <ctd-id nil="true"/>
  <stitch-id nil="true"/>
  <drugbank-id>DB00145</drugbank-id>
  <pdb-id>GLY</pdb-id>
  <actor-id nil="true"/>
  <organism nil="true"/>
  <export type="boolean">true</export>
  <metabolizing-proteins nil="true"/>
  <transporting-proteins nil="true"/>
  <moldb-smiles>NCC(O)=O</moldb-smiles>
  <moldb-formula>C2H5NO2</moldb-formula>
  <moldb-inchi>InChI=1S/C2H5NO2/c3-1-2(4)5/h1,3H2,(H,4,5)</moldb-inchi>
  <moldb-inchikey>DHMQDGOQFOQNFH-UHFFFAOYSA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">75.0666</moldb-average-mass>
  <moldb-mono-mass type="decimal">75.032028409</moldb-mono-mass>
  <origin>Endogenous</origin>
  <state>Solid</state>
  <logp>-3.21</logp>
  <hmdb-id>HMDB00123</hmdb-id>
  <chembl-id>CHEMBL773</chembl-id>
  <chemspider-id>730</chemspider-id>
  <structure-image-file-name nil="true"/>
  <structure-image-content-type nil="true"/>
  <structure-image-file-size type="integer" nil="true"/>
  <structure-image-updated-at type="dateTime" nil="true"/>
  <biodb-id nil="true"/>
  <synthesis-reference>&lt;p&gt;Koichi Niimura, Takako Kawabe, Takao Ando, Kenichi Saito, &amp;#8220;Phenylalanine-glycine compounds having anti-tumor activity, process for preparation thereof, and pharmaceutical composition containing said compounds.&amp;#8221; U.S. Patent US5411964, issued August, 1908.&lt;/p&gt;</synthesis-reference>
  <structure-image-caption nil="true"/>
  <chemdb-id>CHEM003278</chemdb-id>
  <dsstox-id>DTXSID9020667</dsstox-id>
  <toxcast-id nil="true"/>
  <stoff-ident-origin nil="true"/>
  <stoff-ident-id nil="true"/>
  <susdat-id>NS00001575</susdat-id>
  <iupac>2-aminoacetic acid</iupac>
  <moldb-polar-surface-area>63.31999999999999</moldb-polar-surface-area>
  <moldb-refractivity>16.0034</moldb-refractivity>
  <moldb-polarizability>6.647019971293048</moldb-polarizability>
  <moldb-rotatable-bond-count>1</moldb-rotatable-bond-count>
  <moldb-acceptor-count>3</moldb-acceptor-count>
  <moldb-donor-count>2</moldb-donor-count>
  <moldb-pka-strongest-acidic>2.3074568824727444</moldb-pka-strongest-acidic>
  <moldb-pka-strongest-basic>9.240341660583645</moldb-pka-strongest-basic>
  <moldb-physiological-charge>0</moldb-physiological-charge>
  <moldb-number-of-rings>0</moldb-number-of-rings>
  <moldb-alogps-logp>-3.34</moldb-alogps-logp>
  <moldb-alogps-logs>0.87</moldb-alogps-logs>
  <moldb-alogps-solubility>5.52e+02 g/l</moldb-alogps-solubility>
</compound>
