Details
| Stereochemistry | ACHIRAL |
| Molecular Formula | CHO3 |
| Molecular Weight | 61.0168 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | -1 |
SHOW SMILES / InChI
SMILES
OC([O-])=O
InChI
InChIKey=BVKZGUZCCUSVTD-UHFFFAOYSA-M
InChI=1S/CH2O3/c2-1(3)4/h(H2,2,3,4)/p-1
| Molecular Formula | CH2O3 |
| Molecular Weight | 62.0248 |
| Charge | 0 |
| Count |
|
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
DescriptionSources: https://www.drugs.com/dosage/sodium-bicarbonate.htmlhttps://www.ncbi.nlm.nih.gov/pubmed/10932544Curator's Comment: description was created based on several sources, including
https://www.ncbi.nlm.nih.gov/pubmed/26617001 | https://www.ncbi.nlm.nih.gov/pubmed/3449184 | https://www.ncbi.nlm.nih.gov/pubmed/3449184 | https://www.ncbi.nlm.nih.gov/pubmed/16864561
Sources: https://www.drugs.com/dosage/sodium-bicarbonate.htmlhttps://www.ncbi.nlm.nih.gov/pubmed/10932544
Curator's Comment: description was created based on several sources, including
https://www.ncbi.nlm.nih.gov/pubmed/26617001 | https://www.ncbi.nlm.nih.gov/pubmed/3449184 | https://www.ncbi.nlm.nih.gov/pubmed/3449184 | https://www.ncbi.nlm.nih.gov/pubmed/16864561
Diammonium carbonate is a salt with the chemical formula (NH4)2CO3. Since it readily degrades to gaseous ammonia and carbon dioxide upon heating, it is used as a leavening agent and also as smelling salt. Ammonium carbonate may be used as a leavening agent in traditional recipes, particularly those from northern Europe and Scandinavia (e.g. Speculoos, Tunnbröd or Lebkuchen). It also serves as an acidity regulator and has the E number E503. Ammonium carbonate is the main component of smelling salts, although the commercial scale of their production is small. Buckley's cough syrup from Canada today uses ammonium carbonate as an active ingredient intended to help relieve symptoms of bronchitis. Ammonium carbonate is also used as an emetic.
Approval Year
Targets
| Primary Target | Pharmacology | Condition | Potency |
|---|---|---|---|
Target ID: CHEMBL205 Sources: https://www.ncbi.nlm.nih.gov/pubmed/23078755 |
85.0 mM [Ki] | ||
Target ID: CHEMBL261 Sources: https://www.ncbi.nlm.nih.gov/pubmed/15357993 |
12.0 mM [Ki] | ||
Target ID: CHEMBL4789 Sources: https://www.ncbi.nlm.nih.gov/pubmed/15664814 |
95.0 mM [Ki] | ||
Target ID: CHEMBL2326 Sources: https://www.ncbi.nlm.nih.gov/pubmed/16621537 |
0.27 mM [Ki] | ||
Target ID: CHEMBL3594 Sources: https://www.ncbi.nlm.nih.gov/pubmed/15664814 |
0.086 mM [Ki] | ||
Target ID: CHEMBL3025 Sources: https://www.ncbi.nlm.nih.gov/pubmed/21208801 |
0.8 mM [Ki] |
Conditions
| Condition | Modality | Targets | Highest Phase | Product |
|---|---|---|---|---|
| Primary | Unknown Approved UseUnknown |
|||
| Primary | SODIUM BICARBONATE Approved UseINDICATIONS AND USAGE. Sodium Bicarbonate Injection, USP is indicated in the treatment of metabolic acidosis which may occur in severe renal disease, uncontrolled diabetes, circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest and severe primary lactic acidosis. Sodium bicarbonate is further indicated in the treatment of certain drug intoxications, including barbiturates (where dissociation of the barbiturate-protein complex is desired), in poisoning by salicylates or methyl alcohol and in hemolytic reactions requiring alkalinization of the urine to diminish nephrotoxicity of hemoglobin and its breakdown products. Sodium bicarbonate also is indicated in severe diarrhea which is often accompanied by a significant loss of bicarbonate. Launch Date2005 |
|||
| Curative | SODIUM BICARBONATE Approved UseINDICATIONS AND USAGE. Sodium Bicarbonate Injection, USP is indicated in the treatment of metabolic acidosis which may occur in severe renal disease, uncontrolled diabetes, circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest and severe primary lactic acidosis. Sodium bicarbonate is further indicated in the treatment of certain drug intoxications, including barbiturates (where dissociation of the barbiturate-protein complex is desired), in poisoning by salicylates or methyl alcohol and in hemolytic reactions requiring alkalinization of the urine to diminish nephrotoxicity of hemoglobin and its breakdown products. Sodium bicarbonate also is indicated in severe diarrhea which is often accompanied by a significant loss of bicarbonate. Launch Date2005 |
|||
| Primary | SODIUM BICARBONATE Approved UseINDICATIONS AND USAGE. Sodium Bicarbonate Injection, USP is indicated in the treatment of metabolic acidosis which may occur in severe renal disease, uncontrolled diabetes, circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest and severe primary lactic acidosis. Sodium bicarbonate is further indicated in the treatment of certain drug intoxications, including barbiturates (where dissociation of the barbiturate-protein complex is desired), in poisoning by salicylates or methyl alcohol and in hemolytic reactions requiring alkalinization of the urine to diminish nephrotoxicity of hemoglobin and its breakdown products. Sodium bicarbonate also is indicated in severe diarrhea which is often accompanied by a significant loss of bicarbonate. Launch Date2005 |
PubMed
| Title | Date | PubMed |
|---|---|---|
| Does glucose infusion exacerbate metformin-associated lactate acidosis? A case report. | 2009-07 |
|
| Peroxymonocarbonate and carbonate radical displace the hydroxyl-like oxidant in the Sod1 peroxidase activity under physiological conditions. | 2009-04 |
|
| How to explain a PaO2 of 140 mmHg in a venous line? | 2009 |
|
| Gender-specific protection of estrogen against gastric acid-induced duodenal injury: stimulation of duodenal mucosal bicarbonate secretion. | 2008-09 |
|
| Carbonic anhydrase inhibitors: cloning, characterization, and inhibition studies of the cytosolic isozyme III with sulfonamides. | 2007-12-01 |
|
| Comparative transport efficiencies of urea analogues through urea transporter UT-B. | 2007-07 |
|
| DNA cleavage mediated by copper superoxide dismutase via two pathways. | 2007-02 |
|
| ZIP8, member of the solute-carrier-39 (SLC39) metal-transporter family: characterization of transporter properties. | 2006-07 |
|
| Effect of bicarbonate on iron-mediated oxidation of low-density lipoprotein. | 2005-07-26 |
|
| Endothelin-3 applied to the brain evokes opposite effects on bile secretion mediated by a central nitric oxide pathway. | 2005-07 |
|
| Chloride conductance of CFTR facilitates basal Cl-/HCO3- exchange in the villous epithelium of intact murine duodenum. | 2005-06 |
|
| Novel regulation of cystic fibrosis transmembrane conductance regulator (CFTR) channel gating by external chloride. | 2004-10-01 |
|
| Cystic fibrosis gene mutation reduces epithelial cell acidification and injury in acid-perfused mouse duodenum. | 2004-10 |
|
| [HCO3-]-regulated expression and activity of soluble adenylyl cyclase in corneal endothelial and Calu-3 cells. | 2004-04-29 |
|
| Inhibitory regulation of cystic fibrosis transmembrane conductance regulator anion-transporting activities by Shank2. | 2004-03-12 |
|
| NHE3 inhibition activates duodenal bicarbonate secretion in the rat. | 2004-01 |
|
| An alternative mechanism of bicarbonate-mediated peroxidation by copper-zinc superoxide dismutase: rates enhanced via proposed enzyme-associated peroxycarbonate intermediate. | 2003-06-06 |
|
| Acute regulation of the SLC26A3 congenital chloride diarrhoea anion exchanger (DRA) expressed in Xenopus oocytes. | 2003-05-15 |
|
| HCO(3)(-)-dependent soluble adenylyl cyclase activates cystic fibrosis transmembrane conductance regulator in corneal endothelium. | 2003-05 |
|
| Cytokine-stimulated nitric oxide production inhibits adenylyl cyclase and cAMP-dependent secretion in cholangiocytes. | 2003-03 |
|
| Bicarbonate reabsorption and NHE-3 expression: abundance and activity are increased in Henle's loop of remnant rats. | 2002-12 |
|
| [Metformin-associated lactic acidosis with acute renal failure in type 2 diabetes mellitus]. | 2002-02-15 |
|
| Anion exchanger isoform 2 operates in parallel with Na(+)/H(+) exchanger isoform 1 during regulatory volume decrease of human cervical cancer cells. | 2002-02-13 |
|
| Correction of CFTR malfunction and stimulation of Ca-activated Cl channels restore HCO3- secretion in cystic fibrosis bile ductular cells. | 2002-01 |
|
| Role of NHE isoforms in mediating bicarbonate reabsorption along the nephron. | 2001-12 |
|
| Modification of a single tryptophan residue in human Cu,Zn-superoxide dismutase by peroxynitrite in the presence of bicarbonate. | 2001-07-09 |
|
| Proximal renal tubular acidosis secondary to FK506 in pediatric liver transplant patients. | 1995-08 |
|
| Dose-response effects of atropine on pancreatic secretory response to intravenous cerulein in dogs. | 1986 |
|
| Toxic synergism of disopyramide and hyperkalemia. | 1980-10 |
Patents
Sample Use Guides
In cardiac arrest, a rapid intravenous dose of one to two 50 mL syringes (44.6 to 100 mEq) may be given initially and continued at a rate of 50 mL (44.6 to 50 mEq) every 5 to 10 minutes if necessary (as indicated by arterial pH and blood gas monitoring) to reverse the acidosis. Caution should be observed in emergencies where very rapid infusion of large quantities of bicarbonate is indicated. Bicarbonate solutions are hypertonic and may produce an undesirable rise in plasma sodium concentration in the process of correcting the metabolic acidosis. In cardiac arrest, however, the risks from acidosis exceed those of hypernatremia.In less urgent forms of metabolic acidosis. Sodium Bicarbonate Injection, USP may be added to other intravenous fluids. The amount of bicarbonate to be given to older children and adults over a four-to- eight-hour period is approximately 2 to 5 mEq/kg of body weight - depending upon the severity of the acidosis as judged by the lowering of total CO2 content blood pH and clinical condition of the patient In metabolic acidosis associated with shock, therapy should be monitored by measuring blood gases, plasma osmolar'rty, arterial blood lactate, hemodynamics and cardiac rhythm. Bicarbonate therapy should always be planned in a stepwise fashion since the degree of response from a given dose is not precisely predictable. Initially an infusion of 2 to 5 mEq/kg body weight over a period of 4 to 8 hours will produce a measurable improvement in the abnormal acid- base status of the blood. The next step of therapy is dependent upon the clinical response of the patient. If severe symptoms have abated, then the frequency of administration and the size of the dose may be reduced.
Route of Administration:
Intravenous
In Vitro Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/27762345
A. thaliana var. Landsberg erecta (LER) suspension cells were treated with NaHCO3 at a final concentration of 1, 3, or 10 mM. For controls, NaNO3 (NO3 − is a macronutrient in MS media) was added in same concentration to nullify the effect of Na+ during the treatment. Furthermore, as HCO3 − induced significant pH changes of the MS media (pH 5.8), we added 50 mM (for 1 mM and 3 mM HCO3 −) and 100 mM (for 10 mM HCO3 −) MES buffer (pH 5.8) to the MS media, and the pH-stabilized MS media were used for both control and HCO3− treatments. In addition, the buffered MS media were sonicated to remove atmospheric gases prior to addition of HCO3−. Cells were incubated at 25 °C for 0, 5, 15, 30, 60, and 120 min on a shaker, and four replicates (n = 4) were generated for each data point after treatment with HCO3 − (treatment) and control. After treatment, 100 ml cells at a concentration of 3 x 10^6 ml−1 were filtered using filter paper mounted on funnels, quickly blotted dry using Kim wipes and immediately snap-frozen in liquid nitrogen and stored in a − 80 °C freezer until metabolite extraction.
| Substance Class |
Chemical
Created
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| Record UNII |
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21 CFR 331.15
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