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1. Benzoate, Sodium
1. 532-32-1
2. Antimol
3. Sobenate
4. Benzoic Acid, Sodium Salt
5. Benzoic Acid Sodium Salt
6. Sodium;benzoate
7. Benzoate Of Soda
8. Benzoate, Sodium
9. Sodiumbenzoate
10. Fema No. 3025
11. Purox S
12. Fuminaru
13. Microcare Sb
14. Benzoic Acid Sodium
15. Benzoate Sodium
16. Oj245fe5eu
17. E211
18. Ins No.211
19. Ins-211
20. E-211
21. Natrium Benzoicum
22. Caswell No. 746
23. Benzoan Sodny [czech]
24. Benzoan Sodny
25. Fema Number 3025
26. Ccris 3921
27. Hsdb 696
28. Benzoesaeure (na-salz) [german]
29. Benzoesaeure (na-salz)
30. Sodium Benzoate Solution
31. Einecs 208-534-8
32. Mfcd00012463
33. Unii-oj245fe5eu
34. Epa Pesticide Chemical Code 009103
35. Ai3-07835
36. Bzona
37. Sodium Benzoate [usan:jan:nf]
38. Sodium Benzoate Usp
39. Sodium Benzoate,(s)
40. Sodium Benzoate (tn)
41. Dsstox_cid_140
42. Schembl823
43. Ec 208-534-8
44. Chembl1356
45. Dsstox_rid_75393
46. Dsstox_gsid_20140
47. Sodium Benzoate [ii]
48. Sodium Benzoate [mi]
49. Sodium Benzoate (jp17/nf)
50. Sodium Benzoate [fcc]
51. Sodium Benzoate [jan]
52. Sodium Benzoate [fhfi]
53. Sodium Benzoate [hsdb]
54. Sodium Benzoate [inci]
55. Sodium Benzoate [usan]
56. Sodium Benzoate [vandf]
57. Dtxsid1020140
58. Sodium Benzoate [mart.]
59. Sodium Benzoate [usp-rs]
60. Sodium Benzoate [who-dd]
61. Chebi:113455
62. Sodium Benzoate (fragrance Grade)
63. Benzoic Acid, Sodium Salt (1:1)
64. Tox21_300125
65. Sodium Benzoate [orange Book]
66. Akos003053000
67. Akos015890021
68. Sodium Benzoate [ep Monograph]
69. Ccg-266169
70. Ammonul Component Sodium Benzoate
71. Ucephan Component Sodium Benzoate
72. Ncgc00254072-01
73. Cas-532-32-1
74. Sodium Benzoate Component Of Ammonul
75. Sodium Benzoate Component Of Ucephan
76. Ft-0645126
77. S0593
78. Benzoic Acid Sodium 100 Microg/ml In Methanol
79. D02277
80. A829462
81. Q423971
82. J-519752
| Molecular Weight | 144.10 g/mol |
|---|---|
| Molecular Formula | C7H5NaO2 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 2 |
| Rotatable Bond Count | 1 |
| Exact Mass | 144.01872368 g/mol |
| Monoisotopic Mass | 144.01872368 g/mol |
| Topological Polar Surface Area | 40.1 Ų |
| Heavy Atom Count | 10 |
| Formal Charge | 0 |
| Complexity | 108 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 2 |
Antifungal Agents; Food Preservatives
National Library of Medicine's Medical Subject Headings. Sodium Benzoate. Online file (MeSH, 2016). Available from, as of April 27, 2016: https://www.nlm.nih.gov/mesh/2016/mesh_browser/MBrowser.html
Sodium phenylacetate and sodium benzoate is used as adjunctive therapy for the treatment of acute hyperammonemia and associated encephalopathy in patients with disorders (i.e., deficiencies in enzymes) of the urea cycle. Sodium phenylacetate and sodium benzoate is designated an orphan drug by the US Food and Drug Administration (FDA) for this use.
American Society of Health-System Pharmacists 2016; Drug Information 2016. Bethesda, MD. 2016
/EXPL THER/ In addition to dopaminergic hyperactivity, hypofunction of the N-methyl-d-aspartate receptor (NMDAR) has an important role in the pathophysiology of schizophrenia. Enhancing NMDAR-mediated neurotransmission is considered a novel treatment approach. To date, several trials on adjuvant NMDA-enhancing agents have revealed beneficial, but limited, efficacy for positive and negative symptoms and cognition. Another method to enhance NMDA function is to raise the levels of d-amino acids by blocking their metabolism. Sodium benzoate is a d-amino acid oxidase inhibitor. /The objective of this study was/ to examine the clinical and cognitive efficacy and safety of add-on treatment of sodium benzoate for schizophrenia. /The study consisted of/ a randomized, double-blind, placebo-controlled trial in 2 major medical centers in Taiwan composed of 52 patients with chronic schizophrenia who had been stabilized with antipsychotic medications for 3 months or longer. /Interventions included/ six weeks of add-on treatment of 1 g/d of sodium benzoate or placebo. The primary outcome measure was the Positive and Negative Syndrome Scale (PANSS) total score. Clinical efficacy and adverse effects were assessed biweekly. Cognitive functions were measured before and after the add-on treatment. Benzoate produced a 21% improvement in PANSS total score and large effect sizes (range, 1.16-1.69) in the PANSS total and subscales, Scales for the Assessment of Negative Symptoms-20 items, Global Assessment of Function, Quality of Life Scale and Clinical Global Impression and improvement in the neurocognition subtests as recommended by the National Institute of Mental Health's Measurement and Treatment Research to Improve Cognition in Schizophrenia initiative, including the domains of processing speed and visual learning. Benzoate was well tolerated without significant adverse effects. Benzoate adjunctive therapy significantly improved a variety of symptom domains and neurocognition in patients with chronic schizophrenia. The preliminary results show promise for d-amino acid oxidase inhibition as a novel approach for new drug development for schizophrenia.
PMID:24089054 Lane HY et al; JAMA Psychiatry 70 (12): 1267-75 (2013)
/EXPL THER/ N-methyl-D-aspartate receptor (NMDAR)-mediated neurotransmission is vital for learning and memory. Hypofunction of NMDAR has been reported to play a role in the pathophysiology of Alzheimer disease (AD), particularly in the early phase. Enhancing NMDAR activation might be a novel treatment approach. One of the methods to enhance NMDAR activity is to raise the levels of NMDA coagonists by blocking their metabolism. This study examined the efficacy and safety of sodium benzoate, a D-amino acid oxidase inhibitor, for the treatment of amnestic mild cognitive impairment and mild AD. We conducted a randomized, double-blind, placebo-controlled trial in four major medical centers in Taiwan. Sixty patients with amnestic mild cognitive impairment or mild AD were treated with 250-750 mg/day of sodium benzoate or placebo for 24 weeks. Alzheimer's Disease Assessment Scale-cognitive subscale (the primary outcome) and global function (assessed by Clinician Interview Based Impression of Change plus Caregiver Input) were measured every 8 weeks. Additional cognition composite was measured at baseline and endpoint. Sodium benzoate produced a better improvement than placebo in Alzheimer's Disease Assessment Scale-cognitive subscale (p = .0021, .0116, and .0031 at week 16, week 24, and endpoint, respectively), additional cognition composite (p = .007 at endpoint) and Clinician Interview Based Impression of Change plus Caregiver Input (p = .015, .016, and .012 at week 16, week 24, and endpoint, respectively). Sodium benzoate was well-tolerated without evident side-effects. Sodium benzoate substantially improved cognitive and overall functions in patients with early-phase AD. The preliminary results show promise for D-amino acid oxidase inhibition as a novel approach for early dementing processes.
Lin CH et al; Biol Psychiatry 75 (9): 678-85 (2014) 24074637
/EXPL THER/ A recent clinical study demonstrated that sodium benzoate (SB), a prototype competitive d-amino acid oxidase inhibitor, was effective in the treatment of several symptoms, such as positive and negative symptoms, and cognitive impairment in medicated patients with schizophrenia. The objective of the study was to examine the effects of SB on behavioral abnormalities such as pre-pulse inhibition (PPI) deficits and hyperlocomotion in mice after a single administration of the N-methyl-D-aspartate (NMDA) receptor antagonist, phencyclidine (PCP). The effects of SB on behavioral abnormalities (PPI deficits and hyperlocomotion) in mice after PCP administration were examined. Furthermore, effects of SB on tissue levels of amino acids were also examined. A single oral dose of SB (100, 300, or 1000 mg/kg) attenuated PPI deficits in mice after administration of PCP (3.0 mg/kg, s.c.) in a dose-dependent manner. In contrast, L-701,324 (10 mg/kg), an antagonist at the glycine site of the NMDA receptor, did not affect the effect of SB (1000 mg/kg) on PCP-induced PPI deficits. Furthermore, a single oral dose of SB (1000 mg/kg) significantly attenuated the hyperlocomotion in mice after administration of PCP (3.0 mg/kg, s.c.). However, a single oral dose of SB (1000 mg/kg) caused no changes to D-serine levels in plasma or in the frontal cortex, hippocampus, and striatum of these animals. This study suggests that SB induced antipsychotic effects in the PCP model of schizophrenia, although it did not increase D-serine levels in the brain.
PMID:25648314 Matsuura A et al; Acta Neuropsychiatr 27 (3): 159-67 (2015)
At /the therapeutic/ dose level, clinical signs of toxicity are rare and in most cases limited to anorexia and vomiting, especially after intravenous bolus infusions.
International Programme on Chemical Safety's Concise International Chemical Assessment Documents. Number 26: Benzoic Acid and Sodium Benzoate (2000). Available from, as of April 27, 2016: https://www.inchem.org/pages/cicads.html
Antifungal Agents
Substances that destroy fungi by suppressing their ability to grow or reproduce. They differ from FUNGICIDES, INDUSTRIAL because they defend against fungi present in human or animal tissues. (See all compounds classified as Antifungal Agents.)
Food Preservatives
Substances capable of inhibiting, retarding or arresting the process of fermentation, acidification or other deterioration of foods. (See all compounds classified as Food Preservatives.)
A - Alimentary tract and metabolism
A16 - Other alimentary tract and metabolism products
A16A - Other alimentary tract and metabolism products
A16AX - Various alimentary tract and metabolism products
A16AX11 - Sodium benzoate
Overall there are signs of systemic absorption via oral and dermal exposures, no evidence of target organs or of excretion. After oral ingestion and dermal absorption, the test substance will be metabolised to hippuric acid. Despite the low log Pow value, results of the 28-day study in rats and the predicted metabolism do not indicate a potential for the substance to bioaccumulate.
European Chemicals Agency (ECHA); Registered Substances, Sodium benzoate (CAS Number: 532-32-1) (EC Number: 208-534-8) (Last updated: March 18, 2016). Available from, as of April 27, 2016: https://echa.europa.eu/
After oral ingestion of benzoic acid and sodium benzoate, there is a rapid absorption (of undissociated benzoic acid) from the gastrointestinal tract in experimental animals or humans. ... 100% absorption can be assumed. In humans, the peak plasma concentration is reached within 1-2 hr.
International Programme on Chemical Safety's Concise International Chemical Assessment Documents. Number 26: Benzoic Acid and Sodium Benzoate (2000). Available from, as of April 27, 2016: https://www.inchem.org/pages/cicads.html
Hippuric acid is rapidly excreted in urine. In humans, after oral doses of up to 160 mg/kg body weight, 75-100% of the applied dose is excreted as hippuric acid within 6 hr after administration, and the rest within 2-3 days.
International Programme on Chemical Safety's Concise International Chemical Assessment Documents. Number 26: Benzoic Acid and Sodium Benzoate (2000). Available from, as of April 27, 2016: https://www.inchem.org/pages/cicads.html
Experiments on the distribution and elimination of (14)C-benzoate in the rat have shown no accumulation of sodium benzoate or benzoic acid in the body.
International Programme on Chemical Safety's Concise International Chemical Assessment Documents. Number 26: Benzoic Acid and Sodium Benzoate (2000). Available from, as of April 27, 2016: https://www.inchem.org/pages/cicads.html
For more Absorption, Distribution and Excretion (Complete) data for SODIUM BENZOATE (6 total), please visit the HSDB record page.
After oral and dermal uptake, benzoate is metabolized in the liver by conjugation with glycine, resulting in the formation of hippuric acid. The rate of biotransformation in humans is high: after oral doses of 40, 80 or 160 mg sodium benzoate/kg body weight, the transformation to hippuric acid was independent of the dose - about 17-29 mg/kg body weight per hour, corresponding to about 500 mg/kg body weight per day. Other /studies/ obtained higher values of 0.8-2 g/kg body weight per day.
International Programme on Chemical Safety's Concise International Chemical Assessment Documents. Number 26: Benzoic Acid and Sodium Benzoate (2000). Available from, as of April 27, 2016: https://www.inchem.org/pages/cicads.html
Another metabolite of benzoate is the benzoyl glucuronide.
International Programme on Chemical Safety's Concise International Chemical Assessment Documents. Number 26: Benzoic Acid and Sodium Benzoate (2000). Available from, as of April 27, 2016: https://www.inchem.org/pages/cicads.html
The metabolism of the benzoates depletes glycine concentrations and can therefore alter the glycine-dependent metabolism of other compounds. /A study/ demonstrated that ... sodium benzoate successfully competed with aspirin for glycine, resulting in increased concentration and persistence of salicyclic acid in the body.
Cosmetic Ingredient Review; International Journal of Toxicology 20 (Suppl. 3): 23-50 (2001). Available from, as of April 27, 2016: https://www.beauty-review.nl/wp-content/uploads/2014/06/Final-report-on-the-safety-assessment-of-Benzyl-Alcohol-Benzoic-Acid-and-Sodium-Benzoate.pdf
This study underlines the importance of cinnamon, a widely-used food spice and flavoring material, and its metabolite sodium benzoate (NaB), a widely-used food preservative and a FDA-approved drug against urea cycle disorders in humans, in increasing the levels of neurotrophic factors [e.g., brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3)] in the CNS. NaB, but not sodium formate (NaFO), dose-dependently induced the expression of BDNF and NT-3 in primary human neurons and astrocytes. Interestingly, oral administration of ground cinnamon increased the level of NaB in serum and brain and upregulated the levels of these neurotrophic factors in vivo in mouse CNS. Accordingly, oral feeding of NaB, but not NaFO, also increased the level of these neurotrophic factors in vivo in the CNS of mice. NaB induced the activation of protein kinase A (PKA), but not protein kinase C (PKC), and H-89, an inhibitor of PKA, abrogated NaB-induced increase in neurotrophic factors. Furthermore, activation of cAMP response element binding (CREB) protein, but not NF-kappaB, by NaB, abrogation of NaB-induced expression of neurotrophic factors by siRNA knockdown of CREB and the recruitment of CREB and CREB-binding protein to the BDNF promoter by NaB suggest that NaB exerts its neurotrophic effect through the activation of CREB. Accordingly, cinnamon feeding also increased the activity of PKA and the level of phospho-CREB in vivo in the CNS. These results highlight a novel neutrophic property of cinnamon and its metabolite NaB via PKA - CREB pathway, which may be of benefit for various neurodegenerative disorders.
PMID:23475543 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3663914 Jana A et al; J Neuroimmune Pharmacol 8 (3): 739-55 (2013)
DJ-1 (PARK7) is a neuroprotective protein that protects cells from oxidative stress. Accordingly, loss-of-function DJ-1 mutations have been linked with a familial form of early onset Parkinson disease. Mechanisms by which DJ-1 level could be enriched in the CNS are poorly understood. Recently we have discovered anti-inflammatory activity of sodium benzoate (NaB), a metabolite of cinnamon and a widely-used food additive. Here we delineate that NaB is also capable of increasing the level of DJ-1 in primary mouse and human astrocytes and human neurons highlighting another novel neuroprotective effect of this compound. Reversal of DJ-1-inducing effect of NaB by mevalonate, farnesyl phosphate, but not cholesterol and ubiquinone, suggests that depletion of intermediates, but not end products, of the mevalonate pathway is involved in the induction of DJ-1 by NaB. Accordingly, either an inhibitor of p21(ras) farnesyl protein transferase (FPTI) or a dominant-negative mutant of p21(ras) alone was also able to increase the expression of DJ-1 in astrocytes suggesting an involvement of p21(ras) in DJ-1 expression. However, an inhibitor of geranyl geranyl transferase (GGTI) and a dominant-negative mutant of p21(rac) had no effect on the expression of DJ-1, indicating the specificity of the effect. Similarly lipopolysaccharide (LPS), an activator of small G proteins, also inhibited the expression of DJ-1, and NaB and FPTI, but not GGTI, abrogated LPS-mediated inhibition. Together, these results suggest that NaB upregulates DJ-1 via modulation of mevalonate metabolites and that p21(ras), but not p21(rac), is involved in the regulation of DJ-1.
PMID:21701815 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189510 Khasnavis S, Pahan K; J Neuroimmune Pharmacol 7 (2): 424-35 (2012)
This study underlines the importance of cinnamon, a widely-used food spice and flavoring material, and its metabolite sodium benzoate (NaB), a widely-used food preservative and a FDA-approved drug against urea cycle disorders in humans, in increasing the levels of neurotrophic factors [e.g., brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3)] in the CNS. NaB, but not sodium formate (NaFO), dose-dependently induced the expression of BDNF and NT-3 in primary human neurons and astrocytes. Interestingly, oral administration of ground cinnamon increased the level of NaB in serum and brain and upregulated the levels of these neurotrophic factors in vivo in mouse CNS. Accordingly, oral feeding of NaB, but not NaFO, also increased the level of these neurotrophic factors in vivo in the CNS of mice. NaB induced the activation of protein kinase A (PKA), but not protein kinase C (PKC), and H-89, an inhibitor of PKA, abrogated NaB-induced increase in neurotrophic factors. Furthermore, activation of cAMP response element binding (CREB) protein, but not NF-kappaB, by NaB, abrogation of NaB-induced expression of neurotrophic factors by siRNA knockdown of CREB and the recruitment of CREB and CREB-binding protein to the BDNF promoter by NaB suggest that NaB exerts its neurotrophic effect through the activation of CREB. Accordingly, cinnamon feeding also increased the activity of PKA and the level of phospho-CREB in vivo in the CNS. These results highlight a novel neutrophic property of cinnamon and its metabolite NaB via PKA - CREB pathway, which may be of benefit for various neurodegenerative disorders.
PMID:23475543 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3663914 Jana A et al; J Neuroimmune Pharmacol 8 (3): 739-55 (2013)
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