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
Excretion: Excreted by the kidneys; the generated carbon dioxide is expelled through the lungs. Excess sodium bicarbonate is rapidly excreted into the small intestine and absorbed. It is primarily excreted in the urine and effectively alkalizes the urine. …It is completely absorbed after oral administration and is usually excreted within 3-4 hours. Oral administration: Onset of action: rapid; duration of action: 8-10 minutes. Intravenous administration: Onset of action: 15 minutes; duration of action: 1-2 hours. For more complete data on the absorption, distribution, and excretion of sodium bicarbonate (8 items), please visit the HSDB record page. Metabolism/Metabolites Excessive use can cause systemic alkalosis in animals, but the human body normally breaks down bicarbonate ions into water and carbon dioxide… Sodium bicarbonate reacts rapidly with hydrochloric acid to produce sodium chloride, carbon dioxide, and water; excess bicarbonate ions not neutralized by gastric acid are rapidly excreted into the small intestine and absorbed.

Toxicity Summary
Identification and Uses: Sodium bicarbonate is a white crystalline powder or granules. It is used in the manufacture of various sodium salts, as a source of carbon dioxide, and is also an ingredient in baking powder, effervescent salts, and beverages, as well as in fire extinguishers and cleaning agents. It is also used for pH adjustment in analytical chemistry. In the United States, it is used as an anesthetic for fish in aquaculture. Sodium bicarbonate is used to treat metabolic acidosis caused by various diseases. It is also used in veterinary medicine. Human Studies: Risks of acute or chronic oral administration of sodium bicarbonate include metabolic alkalosis, hypernatremia, hypertension, gastric rupture, hyporeninemia, hypokalemia, hypochloremia, intravascular volume depletion, and urinary alkalization. Abrupt cessation of long-term excessive sodium bicarbonate intake may lead to hyperkalemia, hypoaldosteronism, hypovolemia, and calcium and phosphorus metabolism disorders. This study investigated the anticoagulant effect of sodium bicarbonate in fresh human whole blood from healthy volunteers. Prothrombin time and thrombin time assays indicated that sodium bicarbonate interferes with the coagulation process. Animal studies: Sodium bicarbonate is irritating to rabbit eyes. It also showed mild irritation when tested on rabbit skin. This study also evaluated the teratogenicity of sodium bicarbonate at the following maximum doses: mice 580 mg/kg; rats 340 mg/kg; rabbits 330 mg/kg. Results showed that sodium bicarbonate had no teratogenic effect in any of these animals. The mutagenicity of sodium bicarbonate was assessed using metabolically activated Salmonella Typhimurium strains TA 92, TA 94, TA 98, TA 100, TA 1535, and TA 1537 via the Salmonella/microsome assay, with negative results. Ecotoxicity studies: Multiple histological abnormalities, including an increased incidence of necrotic cells, indicate that fish exposed to concentrations >450 mg NaHCO3/L are adversely affected.

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Toxicity Data
LC (Rats) => 900 mg/m3Interactions
Concomitant use of citrate and sodium bicarbonate may promote the formation of calcium stones in patients with uric acid stones, as sodium ions antagonize the hypocalcemic effect of alkaline loading; it may also cause hypernatremia.
Long-term use of sodium bicarbonate with milk or calcium supplements may lead to lactic alkalosis, characterized by hypercalcemia, renal insufficiency, metabolic alkalosis, nausea, vomiting, headache, confusion, and anorexia. In the acute phase of lactic alkalosis, the condition is reversible after discontinuation of calcium and alkaline substances. However, in patients with chronic lactic alkalosis, the decline in renal function may persist even after discontinuation of calcium and alkaline substances. Patients with salt-wasting nephropathy have a higher risk of developing lactic alkalosis.
Concomitant use of anticholinergic drugs or other medications with anticholinergic effects with sodium bicarbonate may reduce absorption, thereby decreasing the efficacy of the anticholinergic drugs; these medications should be taken 1 hour apart from sodium bicarbonate. Furthermore, urine alkalization may delay drug excretion, thus enhancing the side effects of anticholinergic drugs.
Antacids may alkalize urine, counteracting the effects of urine acidifiers (such as ammonium chloride, ascorbic acid, and potassium or sodium phosphate); patients receiving urine acidification therapy should avoid frequent use of antacids, especially in high doses.
For more complete data on interactions of sodium bicarbonate (17 types), please visit the HSDB record page.

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Non-human toxicity values
Oral LD50 in rats: 4,220 mg/kg
Oral LD50 in mice: 3,360 mg/kg

Sodium bicarbonate is an odorless white crystalline powder or lumps, slightly alkaline (bitter taste). A freshly prepared 0.1 mol aqueous solution has a pH of 8.3 (77°F/25°C). A saturated solution has a pH of 8-9. It is non-toxic.
Sodium bicarbonate is an organic sodium salt and a single-carbon compound. It is used as an antacid and a food anti-caking agent. It contains one bicarbonate ion.
Sodium bicarbonate is a white crystalline powder, commonly used as a pH buffer, electrolyte supplement, systemic alkalizer, and external cleanser.
Sodium bicarbonate is the monosodium salt of carbonic acid, possessing alkalizing and electrolyte-supplementing properties. Upon dissociation, sodium bicarbonate produces sodium ions and bicarbonate ions. Ion formation increases plasma bicarbonate concentration and buffers excess hydrogen ions, thereby raising the blood pH.
Soda water is a beverage composed of carbonated water and flavorings.
Sodium bicarbonate is a white crystalline powder, commonly used as a pH buffer, electrolyte supplement, systemic alkalizer, and external cleanser. See also: bicarbonate ions (active moiety); sodium ions (active moiety); omeprazole; sodium bicarbonate (component)... See more...

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Drug Indications
Sodium bicarbonate is used to treat metabolic acidosis, which may occur in severe kidney disease, uncontrolled diabetes, circulatory failure due to shock or severe dehydration, cardiopulmonary bypass, cardiac arrest, and severe primary lactic acidosis. It is also indicated for severe diarrhea, which is often accompanied by significant bicarbonate loss. Sodium bicarbonate is also indicated for the treatment of certain drug poisonings, including barbiturates (when dissociation of barbiturate protein complexes is required), salicylates, or methanol poisoning, and hemolytic reactions requiring alkalization of urine to reduce hemoglobin nephrotoxicity.

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Mechanism of Action
Sodium bicarbonate is a systemic alkalizing agent that increases plasma bicarbonate concentration, buffers excess hydrogen ion concentration, and raises blood pH, thereby reversing the clinical manifestations of acidosis. It is also a urine alkalizing agent, increasing the excretion of free bicarbonate ions in urine, thereby effectively raising the urine pH. By maintaining the urine alkalinity, the actual dissolution of uric acid stones can be achieved. Sodium bicarbonate, as an antacid, neutralizes or buffers existing stomach acid through a chemical reaction, but has no direct effect on its excretion. This effect leads to an increase in the pH of the stomach contents, thereby relieving symptoms of excessive stomach acid. [PharmGKB]

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Therapeutic Uses
Sodium bicarbonate is used to treat metabolic acidosis caused by a variety of diseases, including severe kidney disease (e.g., renal tubular acidosis), uncontrolled diabetes (ketoacidosis), cardiopulmonary bypass, cardiac arrest, circulatory failure due to shock or severe dehydration, ureterosigmoid anastomosis, lactic acidosis, alcoholic ketoacidosis, and administration of carbonic anhydrase inhibitors and ammonium chloride. The main disturbances in metabolic acidosis are proton acceptor loss (e.g., bicarbonate loss during severe diarrhea) or acid load accumulation (e.g., ketoacidosis, lactic acidosis, renal tubular acidosis). The specific role of sodium bicarbonate in the treatment of diabetic ketoacidosis is not yet established. Because correcting the underlying metabolic disturbance usually also corrects acid-base imbalances, and because sodium bicarbonate treatment carries potential risks, its use is generally limited to treating severe acidosis (e.g., arterial blood pH below 7–7.15 or serum bicarbonate concentration below 8 mEq/L). Rapid administration of sodium bicarbonate to correct acidosis in patients with diabetic ketoacidosis may lead to hypokalemia, paradoxical cerebrospinal fluid acidosis (because carbon dioxide diffuses into the cerebrospinal fluid more readily than bicarbonate), and lactic acidosis (because elevated pH increases the oxygen affinity of hemoglobin, and these patients also have a deficiency of erythrocyte 2,3-diphosphoglycerate (2,3-DPG), leading to peripheral tissue hypoxia). However, the benefits and risks of sodium bicarbonate in treating diabetic ketoacidosis are not fully established, and more controlled studies are needed to evaluate the safety and efficacy of this drug. Generally, when using sodium bicarbonate to treat diabetic ketoacidosis, only partial correction of acidosis should be performed (e.g., correcting arterial blood pH to approximately 7.2) to avoid rebound metabolic alkalosis during ketone body metabolism. Oral sodium bicarbonate can be used as an adjunct to uricosuric drugs to reduce uric acid crystals in patients with gout. (This information is included on the US product label.) Injectable sodium bicarbonate is indicated for the treatment of certain drug poisonings, including barbiturate poisoning, as well as salicylate or methanol poisoning. /Included on the US product label/ For more complete data on the therapeutic uses of sodium bicarbonate (29 types), please visit the HSDB record page.

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Drug Warnings
Sodium bicarbonate is generally contraindicated in patients with metabolic or respiratory alkalosis, hypocalcemia (alkalosis may induce tetany), excessive chloride loss due to vomiting or continuous gastrointestinal aspiration, and patients at risk of diuretic-induced hypochloremic alkalosis. Sodium bicarbonate should not be used orally as an antidote for acute ingestion of strong mineral acids, as the neutralization process produces carbon dioxide gas, which may lead to gastric distension and rupture. Sodium bicarbonate should be used with extreme caution in patients with congestive heart failure or other edema or sodium retention; it should also be used with caution in patients with renal insufficiency, especially severe renal insufficiency (e.g., oliguria or anuria), and in patients receiving corticosteroids or adrenocorticotropic hormone (ACTH) therapy, as each gram of sodium bicarbonate contains approximately 12 milliequivalents of sodium. Intravenous administration of sodium bicarbonate may cause fluid and/or solute overload, resulting in serum electrolyte dilution, hydration, congestion, or pulmonary edema. The risks of dilution are inversely proportional to the electrolyte concentration used, while the risks of solute overload and resulting congestion (including peripheral and/or pulmonary edema) are directly proportional to the electrolyte concentration used. Oral administration of sodium bicarbonate may cause flatulence and gastrointestinal flatulence. Accidental extravasation of hypertonic sodium bicarbonate solutions has been reported to cause chemical cellulitis due to its alkalinity, leading to tissue necrosis, ulceration, and/or sloughing at the injection site. Precipitating factors (factors leading to lactic acid syndrome) include: pre-existing hypertension, sarcoidosis, dehydration and electrolyte disturbances (inadequate intravenous infusion) due to vomiting or aspiration of gastric contents, and renal dysfunction due to primary kidney disease. For more complete data on drug warnings for sodium bicarbonate (14 in total), please visit the HSDB record page.

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Pharmacodynamics
Intravenous administration of sodium bicarbonate can increase plasma bicarbonate concentration, buffer excess hydrogen ion concentration, increase blood pH, and reverse 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.)