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| Targets |
The biological target of ABA-GE is not the ABA receptors themselves. ABA-GE is an inactive conjugate that is stored in cellular compartments. Its biological function is achieved after enzymatic hydrolysis to release the active hormone, free abscisic acid (ABA). The hydrolysis is catalyzed by beta-glucosidase enzymes (e.g., AtBG1, AtBG2 in Arabidopsis, and similar enzymes in other plants). Free ABA then binds to its receptors, the PYR/PYL/RCAR family of proteins, which are soluble START-domain proteins. ABA binding to these receptors inhibits the activity of type 2C protein phosphatases (PP2Cs), relieving their repression of SnRK2 kinases. This leads to phosphorylation and activation of downstream transcription factors (e.g., ABI5, AREB/ABF), resulting in stress-responsive gene expression, stomatal closure, and other adaptive responses. Thus, ABA-GE indirectly targets the ABA signaling pathway upon deconjugation.
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| ln Vitro |
In response to abiotic stress conditions like dehydration and salt stress, the endoplasmic reticulum and vacuolar β-glucosidases deconjugate β-D-Glucopyranosyl abscisate (ABA-GE) to facilitate the rapid formation of free ABA. Since β-D-glucopyranosyl abscisate is the main ABA catabolite that is exported from the cytosol, it also helps to maintain ABA homeostasis. In Arabidopsis, β-D-Glucopyranosyl abscisate is transported vacuously through mechanisms involving proton-antiport and ATP-binding cassettes[1].
In vitro, beta-D-Glucopyranosyl abscisate (ABA-GE) is not biologically active in most plant bioassays unless it is hydrolyzed to free ABA. In a seed germination assay, ABA-GE shows only weak ABA-like activity compared to free ABA. While free ABA potently inhibits seed germination at concentrations as low as 0.1-1 uM, ABA-GE requires 10-100 times higher concentrations to achieve the same effect, indicating that its activity is due to minimal spontaneous hydrolysis or the presence of beta-glucosidase activity in the seed. In an ABA-responsive gene expression assay using Arabidopsis protoplasts transfected with an RD29A-LUC reporter, ABA-GE is much less active than ABA, confirming that the conjugate itself is not recognized by ABA receptors. In cell-free assays, ABA-GE is stable and does not directly inhibit PP2C activity or activate SnRK2s. The compound is used as a substrate for purified beta-glucosidases to study ABA deconjugation kinetics. |
| ln Vivo |
In vivo, ABA-GE plays a crucial role in ABA homeostasis and stress responses in plants. In Arabidopsis, ABA-GE accumulates in the vacuole and endoplasmic reticulum under normal conditions. Upon exposure to abiotic stress (drought, salt, cold), ABA-GE is rapidly hydrolyzed by beta-glucosidases (e.g., AtBG1, AtBG2) to release free ABA. This rapid deconjugation allows plants to increase ABA levels within minutes without de novo synthesis, enabling a quick adaptive response. Stress-induced changes in cellular pH may also contribute to hydrolysis. In some plant species, ABA-GE can be transported in the xylem and phloem, serving as a long-distance signaling molecule. Exogenous application of ABA-GE to plants (e.g., by foliar spray or root drench) can induce stress tolerance, but this effect is dependent on the hydrolysis of the conjugate to free ABA. In transgenic plants overexpressing beta-glucosidase genes, ABA-GE levels are lower, and free ABA levels are higher, resulting in enhanced stress tolerance but sometimes stunted growth. Conversely, beta-glucosidase mutants accumulate ABA-GE and exhibit impaired stress responses. ABA-GE is not active in mammalian systems, as mammals do not have ABA receptors.
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| Enzyme Assay |
A non-cellular (cell-free) protocol for evaluating the hydrolysis of ABA-GE by beta-glucosidase uses recombinant AtBG1 enzyme. AtBG1 (Arabidopsis beta-glucosidase 1) is expressed in E. coli and purified by affinity chromatography. The assay buffer is 50 mM sodium acetate (pH 5.0) or 50 mM HEPES (pH 7.0), depending on the pH optimum of the enzyme. For the deconjugation assay, 50 uL of the reaction mixture contains 50 ug of purified AtBG1, 10-500 uM ABA-GE, and assay buffer in a total volume of 100 uL. The reaction is incubated at 30degC for 15-60 minutes. The reaction is terminated by adding 100 uL of 0.1% trifluoroacetic acid (TFA) in acetonitrile. The mixture is centrifuged, and the supernatant is analyzed by reverse-phase HPLC with UV detection at 260 nm (or by LC-MS). A C18 column (e.g., 250 × 4.6 mm) is eluted with a gradient of water (0.1% TFA) and acetonitrile (0.1% TFA) at 1 mL/min. ABA-GE elutes at approximately 8-10 minutes, and free ABA elutes at 12-14 minutes. The amount of ABA released is quantified by comparing peak areas to a standard curve of pure ABA. The enzyme activity (units: nmol ABA released per minute per mg protein) is calculated. To test the effect of inhibitors, add 1 mM gluconolactone or other beta-glucosidase inhibitors to the reaction. The Michaelis-Menten constant (Km) and Vmax for ABA-GE are determined by measuring initial rates at various substrate concentrations (10-500 uM).
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| Cell Assay |
A typical in vitro cellular protocol for evaluating the biological activity of ABA-GE in plants uses an Arabidopsis seed germination assay. Arabidopsis thaliana (wild-type, Col-0) seeds are surface-sterilized with 70% ethanol (1 minute) followed by 20% bleach (10 minutes), then washed five times with sterile distilled water. The seeds are stratified at 4degC for 2-3 days in the dark to break dormancy. For the germination assay, 30-50 seeds are placed onto 9 cm Petri dishes containing 20 mL of 1/2 Murashige and Skoog (MS) medium (0.5× MS salts, 1% sucrose, 0.8% agar, pH 5.7), supplemented with various concentrations of ABA-GE (0.1, 0.5, 1, 5, 10, 25, 50 uM) or free ABA as a positive control (0.1, 0.5, 1 uM). Control plates contain an equivalent volume of solvent (e.g., 0.1% DMSO or ethanol). Seeds are incubated in a growth chamber at 22degC under continuous light (or 16-hour light/8-hour dark). Germination (defined as radicle emergence of 1 mm) is scored daily for 3-7 days. The germination percentage at each concentration is calculated. ABA-GE is expected to have little to no effect on germination at concentrations up to 10 uM unless the seeds have beta-glucosidase activity that converts ABA-GE to ABA. In some seed lots, endogenous beta-glucosidase may cause partial hydrolysis, leading to moderate inhibition at high concentrations (25-50 uM). In comparison, free ABA completely inhibits germination at 0.5-1 uM. This assay is used to characterize mutants in ABA metabolism or beta-glucosidases.
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| Animal Protocol |
An in vivo animal protocol for ABA-GE is not applicable, as the compound is a plant hormone and not intended for animal studies. For plant stress research, an in vivo protocol using Arabidopsis thaliana for evaluating the role of ABA-GE in drought tolerance is described. Arabidopsis plants (wild-type, Col-0) are grown in pots containing a 1:1 mixture of vermiculite and potting mix under controlled conditions (22degC, 16-hour light/8-hour dark, 60% relative humidity) for 4 weeks. One day before the stress treatment, the soil is watered to saturation, and then water is withheld for 10-14 days (drought stress). During the stress period, control plants are watered regularly. To test the effect of ABA-GE application, plants are sprayed with a solution of 10-50 uM ABA-GE in 0.01% Tween-20 (or 0.1% DMSO) at a volume of 10 mL per pot (sufficient to cover the leaves), either 24 hours before drought stress or at the beginning of the stress period. Control plants are sprayed with vehicle only. During the drought stress, the percentage of leaf wilting is recorded daily, and the soil water content is measured gravimetrically. At the end of the stress period (when control plants show severe wilting), plants are rewatered, and survival rates are assessed after 3 days. Leaves are harvested for measurement of free ABA levels (by LC-MS/MS) and expression of stress-responsive genes (e.g., RD29A, RD22, ABF3) by qRT-PCR. ABA-GE treatment is expected to improve drought tolerance if the plant can hydrolyze it to active ABA. However, the effect may be less pronounced than with direct ABA treatment.
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| ADME/Pharmacokinetics |
Pharmacokinetic (PK) data for ABA-GE are relevant only in plants. In plants, ABA-GE is synthesized from ABA by UDP-glucosyltransferases (UGTs), primarily UGT71B6, UGT71C5, and related enzymes. ABA-GE is accumulated in the vacuole and ER, where it is stored as an inactive pool. The half-life of ABA-GE in plant tissues is variable and depends on the activity of beta-glucosidases. In response to stress, ABA-GE can be rapidly hydrolyzed, with free ABA levels rising within minutes. The compound is also transported in the xylem and phloem, allowing for long-distance signaling. In solution, ABA-GE is stable at neutral pH but can be hydrolyzed under acidic conditions. No ADME data are available for mammals, as ABA-GE is not a therapeutic agent for humans.
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| Toxicity/Toxicokinetics |
ABA-GE is a naturally occurring plant metabolite and is not considered toxic to mammals at concentrations typically encountered in the diet. Plants, including many fruits and vegetables, contain ABA-GE as a natural component. Standard laboratory safety precautions should be followed when handling ABA-GE, including the use of gloves, lab coats, and safety glasses. The compound should be stored at -20degC, protected from light and moisture. It is for research use only and is not intended for human therapeutic, diagnostic, or agricultural applications without regulatory approval. As of 2026, ABA-GE has not been approved as a drug or pesticide, although ABA itself is registered as a plant growth regulator in some countries.
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| References | |
| Additional Infomation |
(+)-Abscisic acid β-D-glucopyranose ester is a (+)-abscisic acid D-glucopyranose ester derived from β-D-glucopyranose. Functionally, it is associated with (+)-abscisic acid and β-D-glucopyranose. (+)-Abscisic acid β-D-glucopyranose ester has been reported in Salacia chinensis, Arabidopsis thaliana, and other organisms with relevant data.
beta-D-Glucopyranosyl abscisate (ABA-GE) is an inactive glucose ester conjugate of the plant hormone abscisic acid (ABA). It is the major storage form of ABA in plant cells and is localized in the vacuole and endoplasmic reticulum. Deconjugation by beta-glucosidases (e.g., AtBG1, AtBG2) rapidly releases free ABA in response to abiotic stresses such as drought, high salinity, and low temperature, enabling a quick adaptive response. ABA-GE is also transported in the xylem and phloem, serving as a long-distance signal. The molecular formula is C21H30O9, and the molecular weight is 426.46. The compound is a research tool for studying ABA homeostasis, stress signaling, and plant physiology. It is not approved for human or animal use. |
| Molecular Formula |
C21H30O9
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|---|---|
| Molecular Weight |
426.4575
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| Exact Mass |
426.188
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| CAS # |
21414-42-6
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| PubChem CID |
46173811
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| Appearance |
White to off-white solid
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| LogP |
-0.2
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| Hydrogen Bond Donor Count |
5
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| Hydrogen Bond Acceptor Count |
9
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| Rotatable Bond Count |
6
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| Heavy Atom Count |
30
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| Complexity |
766
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| Defined Atom Stereocenter Count |
6
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| SMILES |
CC1=CC(=O)CC([C@]1(/C=C/C(=C\C(=O)O[C@H]2[C@@H]([C@H]([C@@H]([C@H](O2)CO)O)O)O)/C)O)(C)C
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| InChi Key |
HLVPIMVSSMJFPS-VTEUUMMASA-N
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| InChi Code |
InChI=1S/C21H30O9/c1-11(5-6-21(28)12(2)8-13(23)9-20(21,3)4)7-15(24)30-19-18(27)17(26)16(25)14(10-22)29-19/h5-8,14,16-19,22,25-28H,9-10H2,1-4H3/b6-5+,11-7-/t14-,16-,17+,18-,19+,21-/m1/s1
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| Chemical Name |
[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl] (2Z,4E)-5-[(1S)-1-hydroxy-2,6,6-trimethyl-4-oxocyclohex-2-en-1-yl]-3-methylpenta-2,4-dienoate
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| Synonyms |
ABA-GE; (S)-cis,trans-Abscisic acid glucosyl ester; β-D-Glucopyranosyl abscisate
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: (1). This product requires protection from light (avoid light exposure) during transportation and storage. (2). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO: 50 mg/mL (117.24 mM)
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| Solubility (In Vivo) |
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.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *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). View More
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)] Oral Formulations
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). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.3449 mL | 11.7244 mL | 23.4489 mL | |
| 5 mM | 0.4690 mL | 2.3449 mL | 4.6898 mL | |
| 10 mM | 0.2345 mL | 1.1724 mL | 2.3449 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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