In ginseng (Panax ginseng CA Meyer) adventitious root culture, ethephon (50 μM) can stimulate root growth and ginsenoside accumulation, but at 100 μM, it inhibits ginsenoside accumulation [1].

Absorption, Distribution and Excretion
When fed to lactating cows at a concentration of 5 ppm, a portion of the dose was excreted unchanged in the urine (9.8%), but not detected in milk or feces. Ethylene was detected within 12 hours after application of CEPA to the leaf surfaces of apple and cherry trees. CEPA was also metabolized in the leaves, shells, skin, and kernels of walnuts. Metabolites/Metabolites Plants release ethylene upon contact with CEPA. Phosphates and chlorides were also detected. In the leaf and stem tissues of the Brazilian rubber tree, 2-CEPA was converted into 13 and 20 compounds, respectively. One compound extracted from the stems and leaves was identified as 2-hydroxyethylphosphonic acid. This compound also forms after incubation in a buffer solution for several days at room temperature. In rye, ethephon is metabolized into ethylene and carbon dioxide. In suspension cultures of the Brazilian rubber tree, ethephon is metabolized into multiple compounds. The chromatographic separation results of one of the compounds were similar to those of 2-hydroxyethylphosphonic acid. For more complete metabolite/metabolite data on ethephon (12 metabolites in total), please visit the HSDB record page. Paraoxygenase (PON1) is a key enzyme in organophosphate metabolism. PON1 can inactivate certain organophosphates through hydrolysis. PON1 hydrolyzes active metabolites in a variety of organophosphate pesticides and nerve agents (such as soman, sarin, and VX). The presence of PON1 polymorphism leads to differences in the enzyme activity level and catalytic efficiency of this esterase, which in turn suggests that different individuals may be more susceptible to the toxic effects of organophosphate exposure.

Toxicity Summary
Ethephon is a cholinesterase, or acetylcholinesterase (AChE) inhibitor. Cholinesterase inhibitors (or "anticholinesterases") inhibit the activity of acetylcholinesterase. Because acetylcholinesterase has important physiological functions, chemicals that interfere with its activity are potent neurotoxins; even low doses can cause excessive salivation and lacrimation, followed by muscle spasms, ultimately leading to death. Substances used in nerve gases and many pesticides have been shown to exert their effects by binding to serine residues at the active site of acetylcholinesterase, thus completely inhibiting the enzyme's activity. Acetylcholinesterase breaks down the neurotransmitter acetylcholine, which is released at the neuromuscular junction, causing muscle or organ relaxation. Inhibition of acetylcholinesterase results in the accumulation and sustained action of acetylcholine, leading to the continuous transmission of nerve impulses and the inability to stop muscle contractions. The most common acetylcholinesterase inhibitors are phosphorus-containing compounds, which are designed to bind to the enzyme's active site. Its structural requirements are: a phosphorus atom with two lipophilic groups, a leaving group (e.g., a halide or thiocyanate), and a terminal oxygen atom.

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Toxicity Data
LC50 (rat) = 4,520 mg/m3Interactions
Pretreatment of wild garlic (Allium vineale L.) shoots with low concentrations of 2-chloroethylphosphonic acid (CEPA) increases basal translocation of dicamba after foliar spraying.Ethylene from CEPA alters the metabolic "source-sink" relationship and promotes basal translocation to petals.
Cutting stems of tulip varieties with silver thiosulfate at concentrations of 0.01 to 2.0 μm for 10 minutes to 24 hours completely eliminated the stem elongation inhibition induced by ethylene treatment.
Soaking dormant potato tubers in a mixture of ethylene and gibberellin. The combination of these two substances is more effective at inducing sprouting than either one alone.
The optimal ratio of gibberellin to ethephon is 60:40. Multiple insecticides are widely used for pest control, and the risk of simultaneous exposure to multiple organophosphate compounds is high, especially through dietary and other routes. While the health hazards of individual organophosphate insecticides are well-studied, information on the toxicity of interactions between multiple organophosphate insecticides is relatively limited. This study aimed to investigate the potential interactions between the globally widely used organophosphate insecticide chlorpyrifos and the plant growth regulator ethephon. Ileal segments from 3-month-old Wistar albino male rats were placed in an isolated organ bath containing Tyrode solution. Ethephon and chlorpyrifos (both at 10⁻⁷ M) were incubated separately or in combination in the ileum, and their effects on acetylcholine-induced contractions were investigated. The data obtained in this study indicate that the use of these drugs alone or in combination leads to enhanced acetylcholine potency while decreasing the E(max) value of acetylcholine. These findings suggest that exposure to these drugs with direct and indirect cholinergic effects may induce early clinical responses at low doses, but with low toxicity. This study investigated the effects of subacute combined use of gibberellin and ethephon (2-chloroethylphosphonic acid) on health. Mice were used as the experimental model. Ten groups of male ICR (CD-1) mice were orally administered 25, 50, and 100 mg/kg body weight of gibberellin (GA3), ethephon (2-chloroethylphosphonic acid), or a combination of both for 11 weeks. Results showed that the combined treatment groups had significantly reduced body weight gain and lower dry matter intake in a dose-dependent manner. Statistically significant increases in mean liver, kidney, and spleen weights were observed in all treatment groups. Hemoglobin (Hb) and total erythrocyte count (TEC) decreased in all treatment groups, while total white blood cell count (TLC) increased. Animals treated with gibberellin alone showed the highest liver aspartate aminotransferase (AST) activity, while no significant differences were observed among the other groups. No significant differences were observed in liver alanine aminotransferase (ALT) activity. Highly significant differences were found in serum urea levels among the three treatment groups. No significant differences were found in serum creatinine levels among the three treatment groups. Creatinine levels in all treatment groups were significantly higher than in the control group in a dose-dependent manner. Highly significant dose-dependent differences in acetylcholinesterase (AChE) activity also existed among the treatment groups. The group treated with ethephon alone showed the strongest inhibitory effect on brain acetylcholinesterase (AChE).

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Non-human toxicity values
Oral LD50 in rats: 4000 mg/kg
Dermal LD50 in rabbits: 5730 mg/kg

[1]. Enhanced ginsenoside productivity by combination of ethephon and methyl jasmoante in ginseng (Panax ginseng C.A. Meyer) adventitious root cultures. Biotechnol Lett. 2006 Aug;28(15):1163-6.

(2-Chloroethyl)phosphonic acid is a phosphonic acid compound with a 2-chloroethyl substituent attached to its phosphorus atom. It is a plant growth regulator.
It has been reported that ginkgo contains ethephon, and relevant data is available for reference.
Ethephon is the world's most widely used plant growth regulator, produced by Rhône-Plunkett (Bayer Crop Science). After plants metabolize ethephon, ethylene is converted into ethylene, a potent plant growth and ripening regulator. Ethephon is commonly used in crops such as wheat, coffee, tobacco, cotton, and rice to promote faster fruit ripening. Cotton is the most important single crop application of ethephon. Ethephon can promote cotton fruiting within weeks and promote leaf drop, thereby improving the efficiency of the planned harvest. Pineapple growers also widely use ethephon to promote the reproductive development of pineapples. Ethephon is also often used on ripe green pineapple fruits to dechloroze them to meet the requirements of agricultural product market sales. The toxicity of ethephon is actually very low; any ethephon applied to plants is rapidly converted into ethylene.
Mechanism of Action

A systemic plant growth regulator. It can penetrate plant tissues and decompose into ethylene, thereby affecting plant growth processes. Studies have identified multiple targets of metabolically activated organophosphorus pesticides in both pests and non-target organisms. The high efficiency and specificity of organophosphorus pesticides make them effective chemical probes for studying their mechanisms of action and metabolic processes. Many organophosphorus pesticides have been classified as phosphorylators. Some enzymes inhibited by organophosphorus compounds include acetylcholinesterase, kynurenine formamidinase, neuropathic target esterase, carboxylesterase, and other unknown esterases. Bioactive phosphorylators with sufficient stability to reach organisms while also reacting at the target site have been designed. Most organophosphorus bioactivation is initiated by the oxidation of sulfur or nitrogen linked to phosphorus, but some bioactivation involves the oxidation of carbon or heteroatom centers far from phosphorus. The phosphorus center is not the toxic site of some organophosphorus compounds. The toxic effects of phosphoniminodithiacyclopentane, thiophosphates, and ethephon are mediated by other active groups.
Butyrylcholinesterase (BChE) is inhibited by the plant growth regulator (2-chloroethyl)phosphonic acid (ethephon), a phenomenon that has been confirmed in vitro and in vivo (rat and mouse) and more recently in low-dose subchronic human studies as early as 25 years ago. The currently proposed mechanism is that ethephon divalent anion phosphorylates the S198 site of the BChE active site. This study directly verified this hypothesis using [(33)P]ethephon and recombinant BChE with a single amino acid substitution (rBChE) and further evaluated whether BChE is the most sensitive esterase target in vitro and in vivo (mouse). [(33)P]ethephon can label purified recombinant butyrylcholinesterase (rBChE), but cannot label diethyl phosphate-rBChE (derivatively at S198 after pre-incubation with chlorpyrifos oxyphosphine) or several other esterases and proteins. Amino acid substitutions that significantly reduced rBChE sensitivity to ethephon included G117H and G117K in the oxyanion pores (potentially interfering with the hydrogen bond between glycine-NH and the ethephon divalent anion) and A328F, A328W, and A328Y (potentially hindering entry into the active site canyon). Other substitutions that did not affect sensitivity included D70N, D70K, D70G, and E197Q, which are not directly involved in the catalytic triad. The effects of pH and buffer composition on inhibition supported the hypothesis that the ethephon divalent anion is the actual phosphorylating agent, requiring no activation by the divalent cation. In vitro experiments showed that human plasma butyrylcholinesterase (BChE), and in vitro and in vivo experiments, demonstrated that mouse plasma BChE was more sensitive to ethephon than any other esterase detected by butyrylthiocholine or 1-naphthaleneacetate hydrolysis on native-PAGE. All observed mouse liver esterases were less sensitive to ethephon in vitro and in vivo than plasma BChE. More than ten other esterases are 10-100 times less sensitive to ethephon than BChE. Therefore, BChE inhibition remains the most sensitive marker of ethephon exposure.

C2H6CLO3P

144.49

143.974

16672-87-0

Ethephon-d4;1020719-29-2

27982

White to off-white solid powder

1.6±0.1 g/cm3

333.4±44.0 °C at 760 mmHg

70-72 °C(lit.)

155.4±28.4 °C

0.0±1.5 mmHg at 25°C

1.479

-1.42

2

3

2

7

86.9

0

UDPGUMQDCGORJQ-UHFFFAOYSA-N

InChI=1S/C2H6ClO3P/c3-1-2-7(4,5)6/h1-2H2,(H2,4,5,6)

2-chloroethylphosphonic acid

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: 100 mg/mL (692.09 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.)