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 COW IN DIET @ 5 PPM, SOME OF DOSE WAS EXCRETED UNCHANGED IN URINE (9.8%), BUT NONE WAS PRESENT IN MILK OR FECES.
WITHIN 12 HR AFTER APPLICATION OF CEPA TO LEAF SURFACES OF APPLE & CHERRY TREES, ETHYLENE WAS DETECTED. CEPA IN LEAVES, HULL, SHELL & KERNEL OF WALNUTS WAS ALSO METABOLIZED.

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Metabolism / Metabolites
AFTER EXPOSURE OF PLANTS TO CEPA, ETHYLENE WAS EVOLVED. PHOSPHATE & CHLORIDE WERE ALSO DETECTED.
IN LEAF & STEM TISSUE OF HEVEA BRASILIENSIS, 2-CEPA WAS CONVERTED INTO 13 & 20 COMPD, RESPECTIVELY. ONE OF COMPD OBTAINED FROM STEM & LEAF WAS IDENTIFIED ... AS 2-HYDROXYETHYL-PHOSPHONIC ACID. THIS COMPD ALSO FORMED ... WHEN ... INCUBATED FOR SEVERAL DAYS IN BUFFER SOLN @ ROOM TEMP.
In rye, ethephon was metabolized to ethylene and CO2.
In suspension cultures of Hevea brasiliensis, ethephon was metabolized to a number of compounds. One chromatographed similarly to 2-hydroxy-ethylphosphonic acid.
For more Metabolism/Metabolites (Complete) data for ETHEPHON (12 total), please visit the HSDB record page.
Paraoxonase (PON1) is a key enzyme in the metabolism of organophosphates. PON1 can inactivate some organophosphates through hydrolysis. PON1 hydrolyzes the active metabolites in several organophosphates insecticides as well as, nerve agents such as soman, sarin, and VX. The presence of PON1 polymorphisms causes there to be different enzyme levels and catalytic efficiency of this esterase, which in turn suggests that different individuals may be more susceptible to the toxic effect of OP exposure.

Toxicity Summary
Ethephon is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.

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Toxicity Data
LC50 (rat) = 4,520 mg/m3

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Interactions
PRETREATMENT OF WILD GARLIC (ALLIUM VINEALE L) SHOOTS WITH LOW CONCN OF 2-CHLOROETHYLPHOSPHONIC ACID (CEPA) INCR BASIPETAL TRANSLOCATION OF FOLIAR-APPLIED DICAMBA. ... ETHYLENE FROM CEPA ALTERED METABOLIC "SINK SOURCE" RELATIONSHIPS & PERMITTED INCR BASIPETAL TRANSPORT.
CUT FLOWERINGSTEMS OF TULIPA CULTIVARS WERE TREATED WITH SILVER THIOSULFATE AT 0.01 TO 2.0 MM FOR 10 MIN TO 24 HR. SILVER THIOSULFATE TREATMENT COMPLETELY ABOLISHED INHIBITION OF STEM ELONGATION CAUSED BY TREATMENT WITH ETHEPHON.
DIP TREATMENTS WERE GIVEN TO DORMANT POTATO TUBERS WITH MIXT OF ETHREL & GIBBERELLIC ACID. COMBINATION OF THESE WAS MORE EFFECTIVE FOR SPROUT INDUCTION THAN EITHER APPLIED ALONE. OPTIMUM PROPORTION OF GIBBERELLIN TO ETHREL IS 60-40.
A range of pesticides is widely used in pest management and the chances of exposure to multiple organophosphorus compounds simultaneously are high, especially from dietary and other sources. Although health hazards of individual organophosphorus insecticides have been relatively well characterized, there is lesser information on the interactive toxicity of multiple organophosphorus insecticides. The aim of this study is to elicit the possible interactions in case combined exposure of an organophosphorus pesticide chlorpyrifos and a plant growth regulator ethephon which are used worldwide. The ileum segments of 3 months old Wistar Albino male rats were used in isolated organ bath containing Tyrode solution. Ethephon and chlorpyrifos were incubated (10(-7) M concentration) separately or in combination with each other to ileum and their effects on acetylcholine-induced contractions were studied. The data obtained from this study show that, single and combined exposure to the agents caused agonistic interactions with regard to potency of acetylcholine whereas they caused a decrease on E(max) value of acetylcholine. These findings suggest that exposure to these agents which have direct and indirect cholinergic effects, may cause developing clinical responses with small doses and earlier but the extent of toxicity will be lower.
Health effects of subacute treatment of combinations of gibberellic acid and ethephon (2-chloroethylphosphonic acid) were investigated. Mice was used as an experimental model. Ten groups of male ICR (CD-1) mice were treated with oral doses of 25, 50 and 100 mg of either gibberellic acid (GA3), ethephon (2-chloroethylphosphonic acid) alone or in combination / kg body weight for 11 weeks. A significant dose dependent reduction in weight gain and low dry matter intakes were recorded in animals treated with the combination of both chemicals. Treated groups showed statistically significant increases in mean liver, kidney and spleen weights. Hemoglobin (Hb) and total erythrocyte count (TEC) decreased while total leukocyte count (TLC) was raised in all treated groups. Gibberellic acid (alone) treated animals showed the highest activity of liver aspartate aminotransferase (AST) while no significant variations were recorded among other groups. No significant differences were recorded in the activity of hepatic alanine aminotransferase (ALT). A highly significant variation was recorded among the three treatments in serum urea level. No significant difference was noted among the three treatments in serum creatinine. All treatments caused significant dose dependent increases in creatinine than that of the control group. A highly significant dose dependent variation occurred in acetyl choline esterase (AChE) activity among treated groups. Groups treated with ethephon alone showed the greatest inhibition in brain AChE.

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Non-Human Toxicity Values
LD50 Rat oral 4000 mg/kg
LD50 Rabbit percutaneous 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 having a 2-chloroethyl substituent attached to the P-atom. It has a role as a plant growth regulator.
Ethephon has been reported in Ginkgo biloba with data available.
Ethephon is the word’s most widely used plant growth regulator. It is manufactured by Rhône-Poulenc (Bayer Crop Science). Upon metabolism by the plant, it is converted into ethylene, a potent regulator of plant growth and maturity. It is often used on wheat, coffee, tobacco, cotton, and rice in order to help the plant's fruit reach maturity more quickly. Cotton is the most important single crop use for ethephon. It initiates fruiting over a period of several weeks, and enhances defoliation to facilitate and improve efficiency of scheduled harvesting. Ethephon also is widely used by pineapple growers to initiate reproductive development of pineapple. Ethephon is also sprayed on mature-green pineapple fruits to degreen them to meet produce marketing requirements. The toxicity of ethephon is actually very low, and any ethephon used on the plant is converted very quickly to ethylene.

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Mechanism of Action
Plant growth regulator with systemic properties. Penetrates into the plant tissues, and is decomposed to ethylene, which affects the growth processes.
Studies have established the variety of target sites in pests and nontarget organisms at which the metabolically activated organophosphorus pesticides act. The high potency and specificity of the organophosphorus pesticides have made these cmpd useful chemical probes to further the knowledge of their mode of action and their metabolism. Many organophosphorus pesticides have been classified as phosphorylating agents. Some enzymes inhibited by organophosphorus cmpd have included acetylcholinesterase, kynurenine formamidase, neuropathy-target esterase, carboxyesterases, and other unknown esterases. Bioactive phosphorylating agents have been designed that are sufficiently stable to reach the organism, yet are reactive at the target site. The majority of organophosphorus bioactivations have been initiated by oxidation at sulfur or nitrogen connected to phosphorus, but some bioactivations involve oxidation at carbon or heteroatom centers distant from phosphorus. The phosphorus center is not the toxic site of some organophosphorus cmpd. The toxic effects of phosphinyliminodithiolanes, phosphorothionates, and ethephon are mediated through other reactive moieties.
Butyrylcholinesterase (BChE) is inhibited by the plant growth regulator (2-chloroethyl)phosphonic acid (ethephon) as observed 25 years ago both in vitro and in vivo in rats and mice and more recently in subchronic studies at low doses with human subjects. The proposed mechanism is phosphorylation of the BChE active site at S198 by ethephon dianion. The present study tests this hypothesis directly using [(33)P]ethephon and recombinant BChE (rBChE) with single amino acid substitutions and further evaluates if BChE is the most sensitive esterase target in vitro and with mice in vivo. [(33)P]Ethephon labels purified rBChE but not enzymatically inactive diethylphosphoryl-rBChE (derivatized at S198 by preincubation with chlorpyrifos oxon) or several other esterases and proteins. Amino acid substitutions that greatly reduce rBChE sensitivity to ethephon are G117H and G117K in the oxyanion hole (which may interfere with hydrogen bonding between glycine-N-H and ethephon dianion) and A328F, A328W, and A328Y (perhaps by impeding access to the active site gorge). Other substitutions that do not affect sensitivity are D70N, D70K, D70G, and E197Q which are not directly involved in the catalytic triad. The effect of pH and buffer composition on inhibition supports the hypothesis that ethephon dianion is the actual phosphorylating agent without activation by divalent cations. Human plasma BChE in vitro and mouse plasma BChE in vitro and in vivo are more sensitive to ethephon than any other esterases detected by butyrylthiocholine or 1-naphthyl acetate hydrolysis in native-PAGE. All mouse liver esterases observed are less sensitive than plasma BChE to ethephon in vitro and in vivo. More than a dozen other esterases examined are 10-100-fold less sensitive than BChE to ethephon. Thus, BChE inhibition continues to be 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.)