Absorption, Distribution and Excretion
Animal studies show that bronitropropanol is rapidly absorbed. It can be absorbed via aerosol inhalation, skin contact, and oral administration. In rats, approximately 40% of the topically applied dose of bronitropropanol is absorbed through the skin within 24 hours. After oral administration of 1 mg/kg bronitropropanol to rats, peak plasma concentrations of bronitropropanol are reached within 2 hours. Metabolic studies indicate that bronitropropanol is primarily excreted in the urine. In rats, approximately 19% of dermatically applied bronitropropanol is excreted in urine, feces, and exhaled gases. After oral administration of 1 mg/kg radiolabeled bronitropropanol to rats, approximately 81% and 6% of the administered radioactive material are recovered from urine and exhaled gases, respectively, within 24 hours. After intravenous administration to rats, the recovery rates in urine and exhaled gases are 74% and 9% of the administered dose, respectively. The highest concentrations of bronitropropanol were detected in the excretory organs (such as the kidneys, liver, and lungs) of rats, while the lowest concentrations were found in fat. No data are available. Metabolic data of broonitroxol in rats were obtained from four independent studies using male and female Sprague-Dawley rats. Animals were administered 14C-labeled broonitroxol (radiochemical purity: >95-100%) via gavage. In the first study, animals received a single dose of 10 mg/kg. The second study used a higher dose of 50 mg/kg. Doses exceeding 50 mg/kg resulted in respiratory problems and death. The third study used a dose of 10 mg/kg (14 consecutive days of administration of non-radioactive, 100% pure broonitroxol, followed by a single dose of 14C-labeled broonitroxol). Urine, fecal, and carbon dioxide samples were collected for seven consecutive days following administration, after which rats were sacrificed and their tissues were examined for radioactivity. Since most of the administered 14C is excreted in urine (64-78% within 24 hours and 68-83% within 7 days) regardless of dosage, urine was used for metabolite identification in the fourth study. Feces, carbon dioxide, and tissues are secondary routes of 14C excretion. Trace amounts of 14C were also detected in whole blood and plasma. Based on the results of these four studies… it is concluded that oral administration of bromonitol is rapidly absorbed and excreted in both male and female rats, with urine being the primary route of excretion.
Oral doses are rapidly absorbed and excreted, primarily through urine.
This substance can enter the body via inhaled aerosols, skin absorption, and ingestion.
Approximately 40% of the topically applied antibacterial agent [(14)C]bromonitol ([(14)C]BP) was absorbed through the rat skin within 24 hours. Approximately 19% of the applied radioactive material was excreted through urine, feces, and exhaled gases. Following transdermal administration, the 24-hour recoveries of 14C in urine and exhaled breath were 15% and 2%, respectively; following intravenous administration, the 24-hour recoveries of 14C in urine and exhaled breath were 74% and 9%, respectively. Metabolites/Metabolites Bronitroethanol degrades in aqueous media, reacting with an aldol to form broonitroethanol, releasing an equimolar amount of formaldehyde. Formaldehyde, a degradation product of bronitroethanol, may cause allergic reactions. Broonitroethanol further decomposes into formaldehyde and broonitromethane. Broonitroethanol may also decompose to release nitrite ions and 2-bromoethanol. Approximately 40% of the topical antibacterial agent, 14C-labeled bronitroethanol, was absorbed through the rat skin within 24 hours. Approximately 19% of the administered radioactive material was excreted via urine, feces, and exhaled gases. The 24-hour recoveries of 14C in urine and exhaled gases for the transdermal dose were 15% and 2%, respectively, while those for the intravenous dose were 74% and 9%, respectively. Thin-layer chromatography analysis of urine revealed the presence of three metabolites, but unconverted 14CBP was not detected in either group. These results indicate that rat skin has high permeability to bromonitol. The environmental behavior and toxicological properties of the conversion products often differ from those of the parent contaminant, potentially posing a risk to the environment. This study investigated the toxicological evolution of the unstable preservative bromonitol during its primary degradation in aquatic bodies. Bromonitol rapidly hydrolyzes in natural water bodies, primarily yielding the more stable 2-bromo-2-nitroethanol (BNE) and bromonitromethane (BNM). Irradiation enhanced the degradation of the target compound and exhibited water-site-specific photoactivity. Bond-level analysis theoretically indicated that reversible reverse aldol reactions were the primary degradation pathway for broonitrophenol and BNE. Based on toxicity tests and relative pesticide toxicity indices, these degradation products (i.e., BNE and BNM) are more persistent and toxic than the parent compounds, potentially accumulating in natural water bodies and leading to more severe or persistent adverse effects. Therefore, these transformation products should be considered when assessing the ecological risks of non-persistent and low-toxicity chemicals such as the preservative broonitrophenol. In animals, the major metabolite has been identified as 2-nitropropane-1,3-diol. The only metabolite identified in urine was BTS 23 913 (2-nitropropane-1,3-diol or debromobromophenol), accounting for 45-50% of the radioactivity used in the analysis. The remaining radioactivity was not identified (only one radioactive peak was observed, and the radioactivity was not separated into peaks). Unaltered broonitrophenol was not detected. Nitrosamines can enter the human body through ingestion, inhalation, or skin contact. Once inside, they are metabolized by cytochrome P-450 enzymes, transforming into carcinogens. Sarcosine is metabolized to glycine by sarcosine dehydrogenase. Formaldehyde can be absorbed through inhalation, oral ingestion, or skin contact. It is an essential metabolic intermediate in all cells, produced during the normal metabolism of serine, glycine, methionine, and choline, and can also be produced through the demethylation of N-, S-, and O-methyl compounds. Exogenous formaldehyde is metabolized to formic acid by formaldehyde dehydrogenase at the initial site of exposure. After oxidation to formic acid, the carbon atoms are further oxidized to carbon dioxide, or incorporated into purines, thymidines, and amino acids via a tetrahydrofolate-dependent one-carbon biosynthesis pathway. Formaldehyde is not stored in the body but is excreted in urine (mainly as formic acid), incorporated into other cellular molecules, or exhaled as carbon dioxide. (A2878, A2879, L1892, L962)

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Biological Half-Life
The half-life of broonitropropanol in biological systems has not been reported in the literature. The reported half-lives of broonitropropanol reflect its environmental fate. When released into the air as vapor, broonitropropanol reacts with photochemically generated hydroxyl radicals and degrades in the atmosphere; the half-life of this reaction is approximately 11 days. In water, the photodegradation half-life is 24 hours, but can be as long as 2 days under natural sunlight.

Toxicity Summary
While bromonitrobanol itself is not a nitrosating agent, under decomposition conditions (alkaline solution and/or high temperature), it releases nitrites and low concentrations of formaldehyde. These decomposition products can react with any secondary amine or amide (which may contaminate cosmetics) to generate large amounts of nitrosamines, which are considered carcinogenic. Once in the body, nitrosamines are activated by cytochrome P-450 enzymes. They are subsequently believed to exert their carcinogenic effects by forming adducts on the nitrogen and oxygen atoms of DNA. Formaldehyde itself is also carcinogenic. Formaldehyde toxicity likely occurs when intracellular formaldehyde concentrations saturate with formaldehyde dehydrogenase activity, allowing unmetabolized, intact formaldehyde molecules to exert their effects. Formaldehyde is known to form cross-links between proteins and DNA and is metabolized and integrated into macromolecules (DNA, RNA, and proteins). (L962, L643, L1889, A2878, A2879, A2880, A2881, L1893)

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Protein binding
No data available.

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Toxicity Data
LD50: 250 mg/kg (oral, dog) (A547)
LD50: 64-160 mg/kg (dermal, rat) (A546)
LC50: >5 mg/L (6 hours) (inhalation, rat) (A547)

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Non-human Toxicity Values
Oral LD50 in mice: 350 mg/kg
Oral LD50 in female rats: 342 mg/kg
Oral LD50 in male rats: 307 mg/kg
LD50 in male rats: dermal contact dose 64-160 mg/kg
For more complete non-human toxicity data for BRONOPOL (6 of them), please visit the HSDB record page.

Pharmacodynamics
Bronitroethanol exhibits inhibitory activity against a variety of Gram-negative and Gram-positive bacteria in vitro at concentrations ranging from 12.5 to 50 μg/mL. It has been reported to have stronger bactericidal activity against Gram-negative bacteria than against Gram-positive cocci. Bronitroethanol has also been shown to be effective against a variety of fungi, but its inhibitory effect is weaker compared to its inhibitory effect on bacteria. The inhibitory activity of bronitroethanol decreases with increasing pH of the culture medium. Bronitroethanol also exhibits antiprotozoan activity, which has been demonstrated in vitro and in vivo against Ichthyophthirius multifiliis. It is speculated that bronitroethanol affects the survival of all free-living stages of Ichthyophthirius multifiliis.

C3H6BRNO4

199.99

198.948

52-51-7

Bronopol-d4

2450

White crystalline powder
Crystals from ethyl acetate-chloroform

2.0±0.1 g/cm3

358.0±42.0 °C at 760 mmHg

130-133 °C(lit.)

170.3±27.9 °C

0.0±1.8 mmHg at 25°C

1.575

1.72

2

4

2

9

107

0

OCC([N+]([O-])=O)(Br)CO

LVDKZNITIUWNER-UHFFFAOYSA-N

InChI=1S/C3H6BrNO4/c4-3(1-6,2-7)5(8)9/h6-7H,1-2H2

2-bromo-2-nitropropane-1,3-diol

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

H2O : ~100 mg/mL (~500.03 mM)
DMSO : ~100 mg/mL (~500.03 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (12.50 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (12.50 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
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.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (12.50 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 50 mg/mL (250.01 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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