For life science-related research, monosodium carbonate, 99.5%, is a biochemical reagent that can be utilized as an organic substance or biological material.

Absorption, Distribution and Excretion
Elimination: Renal; carbon dioxide formed is eliminated via lungs.
Excess sodium bicarbonate is emptied rapidly into small intestine where it is absorbed.
It is eliminated principally in the urine and effectively alkalizes it. ... /It/ is completely absorbed orally and usually is excreted within 3-4 hr.
Oral: Onset of action: Rapid; Duration: 8-10 minutes. I.V: Onset of action: 15 minutes; duration: 1-2 hours.
For more Absorption, Distribution and Excretion (Complete) data for Sodium bicarbonate (8 total), please visit the HSDB record page.

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Metabolism / Metabolites
Excessive use can cause systemic alkalosis /in animals/, but body usually splits bicarbonate radical into water and carbon dioxide ...
Sodium bicarbonate rapidly reacts with hydrochloric acid to form sodium chloride, carbon dioxide, and water; excess bicarbonate that does not neutralize gastric acid rapidly empties into the small intestine and is absorbed.

Toxicity Summary
IDENTIFICATION AND USE: Sodium bicarbonate is a white crystalline powder or granules. It is used in manufacturing many sodium salts, as a source of carbon dioxide, ingredient of baking powder, and effervescent salts and beverages, in fire extinguishers, cleaning compounds. It is also used in analytical chemistry for pH adjustment. It is used in aquaculture as an anesthetic for fish in the United States. Sodium bicarbonate is used in the treatment of metabolic acidosis associated with many conditions. It is also used in veterinary medicine. HUMAN STUDIES: Risks of acute and chronic oral bicarbonate ingestion include metabolic alkalosis, hypernatremia, hypertension, gastric rupture, hyporeninemia, hypokalemia, hypochloremia, intravascular volume depletion, and urinary alkalinization. Abrupt cessation of chronic excessive bicarbonate ingestion may result in hyperkalemia, hypoaldosteronism, volume contraction, and disruption of calcium and phosphorus metabolism. The anticoagulant effects of sodium bicarbonate was investigated in fresh human whole blood obtained from normal healthy volunteers. Prothrombin and thrombin clotting time determination indicated that bicarbonate can interfere with the clotting process. ANIMAL STUDIES: Sodium bicarbonate was irritating to the rabbit eye. It was slightly irritating when tested on the skin of rabbits. Sodium bicarbonate was evaluated for teratological effects, maximum dose levels were as follows: mice, 580 mg/kg; rats, 340 mg/kg; and rabbits, 330 mg/kg. No effects were found in any of these species. The mutagenicity of sodium bicarbonate was assessed in Salmonella/microsome assays using Salmonella typhimurium strains TA 92, TA 94, TA 98, TA 100, TA 1535 and TA 1537 with metabolic activation, and it was negative. ECOTOXICITY STUDIES: Several histological anomalies, including increased incidence of necrotic cells, suggested that fish were adversely affected as a result of exposure to >450 mg NaHCO3/L.

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Toxicity Data
LC (rat) = > 900 mg/m3

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Interactions
Concurrent use /of citrates/ with sodium bicarbonate may promote the development of calcium stones in patients with uric acid stones, due to sodium ion opposition to the hypocalciuric effect of the alkaline load; may also cause hypernatremia.
Chronic administration of bicarbonate with milk or calcium may cause the milk-alkali syndrome which is characterized by hypercalcemia, renal insufficiency, metabolic alkalosis, nausea, vomiting, headache, mental confusion, and anorexia. During the acute phase of the milk-alkali syndrome, the condition is reversible when the calcium and alkali are withdrawn. However, in patients with chronic milk-alkali syndrome, reduced renal function may persist even after calcium and alkali are discontinued. Patients with a salt-losing nephropathy have an increased risk of developing the milk-alkali syndrome.
Concurrent use /of anticholinergics or other medications with anticholinergic action/ with sodium bicarbonate may decrease absorption, reducing the effectiveness of the anticholinergic; doses of these medications should be spaced 1 hour apart from doses of sodium bicarbonate; also, urinary excretion may be delayed by alkalinization of the urine, thus potentiating the side effects of the anticholinergic
Antacids may alkalinize the urine and counteract the effect of urinary acidifiers /such as ammonium chloride, ascorbic acid and potassium or sodium phosphates/; frequent use of antacids, especially in high doses, is best avoided by patients receiving therapy to acidify the urine.
For more Interactions (Complete) data for Sodium bicarbonate (17 total), please visit the HSDB record page.

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Non-Human Toxicity Values
LD50 Rat oral 4,220 mg/kg
LD50 Mouse oral 3360 mg/kg

Sodium bicarbonate appears as odorless white crystalline powder or lumps. Slightly alkaline (bitter) taste. pH (of freshly prepared 0.1 molar aqueous solution): 8.3 at 77 °F. pH (of saturated solution): 8-9. Non-toxic.
Sodium hydrogencarbonate is an organic sodium salt and a one-carbon compound. It has a role as an antacid and a food anticaking agent. It contains a hydrogencarbonate.
Sodium bicarbonate is a white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions.
Sodium Bicarbonate is the monosodium salt of carbonic acid with alkalinizing and electrolyte replacement properties. Upon dissociation, sodium bicarbonate forms sodium and bicarbonate ions. Ion formation increases plasma bicarbonate and buffers excess hydrogen ion concentration, resulting in raised blood pH.
Soda is a beverage consisting of carbonated water and a flavoring.
A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions.
See also: Bicarbonate Ion (has active moiety); Sodium Cation (has active moiety); Omeprazole; Sodium Bicarbonate (component of) ... View More ...

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Drug Indication
Sodium bicarbonate is used for 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. Also is indicated in severe diarrhea which is often accompanied by a significant loss of bicarbonate. Further indicated in the treatment of certain drug intoxications, including barbiturates (where dissociation of the barbiturateprotein complex is desired), in poisoning by salicylates or methyl alcohol and in hemolytic reactions requiring alkalinization of the urine to diminish nephrotoxicity of blood pigments.

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Mechanism of Action
Sodium bicarbonate is a systemic alkalizer, which increases plasma bicarbonate, buffers excess hydrogen ion concentration, and raises blood pH, thereby reversing the clinical manifestations of acidosis. It is also a urinary alkalizer, increasing the excretion of free bicarbonate ions in the urine, thus effectively raising the urinary pH. By maintaining an alkaline urine, the actual dissolution of uric acid stones may be accomplished. Sodium bicarbonate acts as an antacid and reacts chemically to neutralize or buffer existing quantities of stomach acid but has no direct effect on its output. This action results in increased pH value of stomach contents, thus providing relief of hyperacidity symptoms. [PharmGKB]

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Therapeutic Uses
Sodium bicarbonate is used in the treatment of metabolic acidosis associated with many conditions including severe renal disease (e.g., renal tubular acidosis), uncontrolled diabetes (ketoacidosis), extracorporeal circulation of the blood, cardiac arrest, circulatory insufficiency caused by shock or severe dehydration, ureterosigmoidostomy, lactic acidosis, alcoholic ketoacidosis, use of carbonic anhydrase inhibitors, and ammonium chloride administration. In metabolic acidosis, the principal disturbance is a loss of proton acceptors (e.g., loss of bicarbonate during severe diarrhea) or accumulation of an acid load (e.g., ketoacidosis, lactic acidosis, renal tubular acidosis).
The specific role of sodium bicarbonate therapy in the treatment of diabetic ketoacidosis has not been established. Because correction of the underlying metabolic disorder generally results in correction of acid-base abnormalities and because of the potential risks of sodium bicarbonate therapy in the treatment of this disorder, administration of sodium bicarbonate is generally reserved for the treatment of severe acidosis (e.g., arterial pH less than 7-7.15 or serum bicarbonate concentration of 8 mEq/L or less). Rapid correction of acidosis with sodium bicarbonate in patients with diabetic ketoacidosis may cause hypokalemia, paradoxical acidosis in cerebrospinal fluid (CSF) since carbon dioxide diffuses more rapidly into CSF than does bicarbonate, and lactic acidosis since increased pH increases hemoglobin-oxygen affinity which, when combined with erythrocyte 2,3-diphosphoglycerate (2,3-DPG) deficiency in these patients, results in peripheral tissue hypoxia. However, the benefits and risks of sodium bicarbonate therapy in ketoacidosis have not been fully determined, and additional controlled studies of the safety and efficacy of the drug are necessary. Generally, when sodium bicarbonate is used in the treatment of diabetic ketoacidosis, the acidosis should only be partially corrected (e.g., to an arterial pH of about 7.2) to avoid rebound metabolic alkalosis as ketones are metabolized.
Oral sodium bicarbonate is indicated to reduce uric acid crystallization as an adjuvant to uricosuric medication in gout. /Included in US product labeling/
Parenteral sodium bicarbonate is indicated in the treatment of certain drug intoxications, including barbiturates, and in poisoning by salicylates or methyl alcohol. /Included in US product labeling/
For more Therapeutic Uses (Complete) data for Sodium bicarbonate (29 total), please visit the HSDB record page.

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Drug Warnings
Sodium bicarbonate is generally contraindicated in patients with metabolic or respiratory alkalosis, in patients with hypocalcemia in whom alkalosis may induce tetany, in patients with excessive chloride loss from vomiting or continuous GI suctioning, and in patients at risk of developing diuretic-induced hypochloremic alkalosis. Sodium bicarbonate should not be used orally as an antidote in the treatment of acute ingestion of strong mineral acids, since carbon dioxide gas forms during neutralization and may cause gastric distention and possible rupture.
Sodium bicarbonate should be used with extreme caution in patients with congestive heart failure or other edematous or sodium-retaining conditions; in patients with renal insufficiency, especially those with severe insufficiency such as oliguria or anuria; and in patients receiving corticosteroids or corticotropin, since each gram of sodium bicarbonate contains about 12 mEq of sodium. IV administration of sodium bicarbonate may cause fluid and/or solute overload resulting in dilution of serum electrolytes, overhydration, congestive conditions, or pulmonary edema. The risk of dilutional conditions is inversely proportional to the electrolyte concentration administered, and the risk of solute overload and resultant congestive conditions with peripheral and/or pulmonary edema is directly proportional to the electrolyte concentration administered.
Gastric distention and flatulence may occur when sodium bicarbonate is administered orally. Inadvertent extravasation of hypertonic solutions of sodium bicarbonate has reportedly caused chemical cellulitis because of their alkalinity, subsequently resulting in tissue necrosis, ulceration, and/or sloughing at the site of injection.
Predisposing factors /contributing to milk-alkali syndrome/ are preexisting hypertension, sarcoidosis, dehydration and electrolyte imbalance due to vomiting or aspiration of gastric contents with inadequate iv fluid replacement, and renal dysfunction caused by primary renal disease.
For more Drug Warnings (Complete) data for Sodium bicarbonate (14 total), please visit the HSDB record page.

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Pharmacodynamics
Intravenous sodium bicarbonate therapy increases plasma bicarbonate, buffers excess hydrogen ion concentration, raises blood pH and reverses the clinical manifestations of acidosis.

CHNAO3

84.0

83.982

144-55-8

7542-12-3 (unspecified hydrochloride salt)

516892

White to off-white solid powder

2.16 g/mL at 25 °C(lit.)

851°C

270 ºC

169.8ºC

2.58E-05mmHg at 25°C

1.500

1

3

0

5

33.9

0

UIIMBOGNXHQVGW-UHFFFAOYSA-M

InChI=1S/CH2O3.Na/c2-1(3)4;/h(H2,2,3,4);/q;+1/p-1

sodium;hydrogen carbonate

Soda Mint Sodium hydrocarbonateSodium bicarbonate NSC-134031 NSC 134031 NSC134031Bicarbonate of soda

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~50 mg/mL (~595.17 mM)

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)