Sodium butyrate

110.09

110.034370

3629439

205-857-6

8RAS91C36W

DTXSID3037672

C2337

2915600000

40.1

-3.2 (LogP)

White Amorphous Powder

0.987g/cm3

251 °C

164.3°C at 760 mmHg

69.7ºC

H2O: soluble

-20°C

1.35mmHg at 25°C

Combustible, the fire emits spicy sodium oxide to stimulate the smoke

2820

1

36/37/38-68

37/39-26-24/25-36/37

ET6400000

Xi,Xn

Warehouse low temperature, ventilated, dry

Stable. Incompatible with strong acids.

P305 + P351 + P338

H315-H319-H335

UN 2820

P305 + P351 + P338

THE INDUCTION OF HELA CELL ALKALINE PHOSPHATASE ACTIVITY BY SODIUM BUTYRATE COULD BE INHIBITED BY THE COADMINISTRATION OF CAFFEINE OR THEOPHYLLINE.|SODIUM BUTYRATE AND DIMETHYL SULFOXIDE HAD MARKED EFFECTS ON THE GROWTH, MORPHOLOGY, AND BIOCHEMISTRY OF 2 HUMAN COLONIC ADENOCARCINOMA CELL LINES IN CULTURE. DOUBLING TIMES WERE INCR BETWEEN 18% & 660% WHEREAS CELL VIABILITY WAS UNAFFECTED.|SODIUM BUTYRATE TOGETHER WITH INTERFERON ENHANCED THE ANTITUMOR EFFECT OF INTERFERON IN VIVO. WHEN SARCOMA 180 TG CELLS WERE INOCULATED IN MICE, THE MEAN SURVIVAL TIME AND FINAL SURVIVAL RATE WERE GREATLY INCR COMPARED TO THOSE TREATED WITH INTERFERON ALONE.|THE COMBINATION OF THE SODIUM BUTYRATE WITH A THERAPEUTIC AGENT (X-RAYS, FLUOROURACIL, LOMUSTINE, VINCRISTINE, ADRIAMYCIN SULFATE, 5-(3,3-DIMETHYL-1-TRIAZENO)IMIDAZOLE-4-CARBOXAMIDE, OR METHOTREXATE) OR A CYCLIC AMP-STIMULATING AGENT (RO 20-1724, THEOPHYLLINE, PAPAVERINE, OR PROSTAGLANDIN E1) RESULTED IN A GREATER REDUCTION OF THE CELL NUMBER IN MOUSE NEUROBLASTOMA CULTURES THAN THAT OBSERVED WITH EACH AGENT ALONE.|Epstein-Barr virus producer and nonproducer cell lines were treated with a combination of phorbol 12-myristate 13-acetate and n-butyrate (sodium salt). These inducers caused a massive hypomethylation of the Epstein-Barr virus producer line P3HR-1 DNA (approx 30%) at the time when DNA replication was inhibited.

Drugs that bind to but do not activate histamine receptors, thereby blocking the actions of histamine or histamine agonists. Classical antihistaminics block the histamine H1 receptors only. (See all compounds classified as Histamine Antagonists.)

Since cancer may be regarded as a disease of differentiation and sodium butyrate induces differentiation of malignant cells in vitro, a study of the clinical pharmacology of sodium butyrate was undertaken. Nine patients with acute myeloid (n= 1), acute monocytic (n= 1), acute myelomonocytic (n= 6) and acute undifferentiated (n= 1) leukemia were treated. Their median age was 52 (range, 27-78) years. Six of the nine patients were pretreated with cytostatic agents. Sodium butyrate was administered iv at a dosage of 500 mg/kg/day as continuous infusion over 10 days. A sensitive and reproducible high-performance liquid chromatographic separation was developed after derivatization of sodium butyrate with 2,4'-dibromoacetophenone employing crown ether catalysts. Plasma concentrations and urinary excretion of sodium butyrate were monitored during the 10 days of continous infusion and for 2 days thereafter. During infusion, plasma concentrations increased 6-fold over the endogenous butyrate level and reached 39-59 uM. The area under the curve of the exogenous butyrate was 384 + or - 50 uM X day (mean + or - standard deviation). After the end of infusion, concentrations declined rapidly with a half-life of 6.1 + or - 1.4 min, and reached pretreatment values within 1 hr. The total clearance rate was 83 + or - 12 ml/kg/min and the volume of distribution 738 + or - 245 ml/kg. The excreted amounts of butyrate in the urine were minmal as compared to the infused dose. Although excretion by other organs was not ruled out, it is suggested that the infused sodium butyrate was rapidly metabolized. A significant increase in peripheral blast cells was observed, whereas bone marrow cytologies before and after treatment did not reveal a significant change in blasts. Differential counts of peripheral white blood cells did not show significantly changes. No toxicity was encountered. The apparent lack of clinical efficacy may be explained by the low plasma levels of sodium butyrate due to its short half-life in vivo. In comparison, concentrations reported for in vitro studies were at least 10 times higher.

SODIUM BUTYRATE INHIBITED INITIATION OF VIRAL AND CELLULAR DNA REPLICATION IN POLYOMA VIRUS-INFECTED MOUSE KIDNEY CELLS.|24 HR AFTER TREATMENT OF FRIEND ERYTHROLEUKEMIA CELLS WITH MILLIMOLAR CONCN OF SODIUM BUTYRATE, THE CHROMATIN HISTONES HAD BECOME HYPERACETYLATED. DURING THIS SAME TIME PERIOD, THE BUTYRATE-TREATED FRIEND CELLS ACCUMULATED A POPULATION OF APPROX 38% NEW RNA TRANSCRIPTS SYNTHESIZED FROM UNIQUE SEQUENCES OF MOUSE DNA.|F9 mouse teratocarcinoma stem cells differentiate into parietal endoderm cells in the presence of retinoic acid, dibutyryl cyclic AMP, and theophylline. When F9 cells are exposed to 2-5 mM sodium butyrate plus retinoic acid, dibutyryl cyclic AMP, and theophylline, they fail to differentiate. Butyrate inhibits differentiation only when added within 8 hr after retinoic acid addition. Thus an early event in retinoid action on F9 cells is butyrate-sensitive. Butyrate inhibits histone deacetylation in F9 cells, and this could be the mechanism by which butyrate inhibits differentiation.|Sodium butyrate treatment enhanced the development of colonic neoplasia and was associated with increased fecal butyric acid concentrations in rats given parenteral administration of 1,2-dimethylhydrazine.|Inhibitors of DNA polymerase efficiently inhibit initiator induced amplification of SV40 DNA sequences in the SV40 transformed Chinese hamster cell line CO631. Sodium butyrate inhibits DNA synthesis by histone modification.

GROWTH OF HUMAN CHRONIC MYELOGENOUS LEUKEMIA K562 CELLS WAS INHIBITED 50% BY SODIUM BUTYRATE (1 MMOLAR); NO DIFFERENTIATION OF THE CELLS WAS DETECTABLE.

Acid, Butanoic

Paper manufacturing|Butanoic acid, sodium salt (1:1): ACTIVE

NIOSH Method 7300. Analyte: Sodium. Matrix: Air. Procedure: Inductively coupled argon plasma, atomic emission spectroscopy. For sodium this method has an estimated detection limit of 1 ug/sample. The precision/RSD and the recovery are not given. Applicability: The working range of this method is 0.005 to 2.0 mg/cu m for each element in a 500 liter air sample. Interferences: Spectral interferences. /Sodium/|Method 3111: Metals A. Direct Aspiration Atomic Absorption Spectrometry is used for the determination of sodium in water and wastewater. Using air-acetylene as the flame gas at a wavelength of 589.0 nm, the detection limit is 0.002 mg/l, with a sensitivity of 0.015 mg/l, at an optimum concentration range of 0.03-1 mg/l. /Sodium/|Method 305: Emission spectroscopy for the determination of sodium in water and wastewater samples. Using an inductively coupled plasma source at a wavelength of 589.0 nm, the detection limit is 30 ug/l. /Sodium/|EPA Method 7770. Atomic Absorption, Direct Aspiration for the determination of sodium in solution. Preliminary treatment of waste water, ground water, Extraction Procedure extracts, and industrial waste is always necessary because of the complexity and variability of the sample matrix. The performance characteristics for an aqueous sample free of interferences are the following: an optimum concentration range of 0.03-1 mg/l with a wavelength of 589.6 nm, a sensitivity of 0.002 mg/l, and a detection limit of 0.015 mg/l. Sodium is a universal contaminant, great care should be taken to avoid contamination. /Sodium/

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