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| Other Sizes |
| Targets |
β-Endorphin (30-31) (human) does not have a classical drug target like a receptor. Instead, it functions as a neurotrophic factor that maintains AChE content and activity. It is also known that β-endorphin can bind to serum glycoproteins, and Gly-Glu competes for these binding sites. Its primary role is in neuroprotection and maintenance of neuronal function, specifically by preserving cholinergic enzyme activity and preventing neuronal degeneration.
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| ln Vitro |
In the clonal neuroblastoma-glioma hybrid NG108-15 cell line, treatment with β-Endorphin (30-31) (human) (glycyl-L-glutamine, GLG) at concentrations of 10^-6, 10^-5, and 10^-4 M did not alter the rate of regeneration of acetylcholinesterase (AChE) activity following irreversible inhibition by soman (5.5 × 10^-6 M for 15 min). AChE activity remained near zero for up to 5 hr post-soman, gradually returned to untreated cell levels at about 20 hr (t1/2 approximately 10 hr), and β-Endorphin (30-31) (human) did not significantly accelerate this recovery at any concentration tested. At early time points (1 and 5 hr), the 10^-5 M group showed slightly higher activity but not sustained. Cycloheximide (2 μg/ml) completely blocked AChE regeneration, indicating dependence on de novo protein synthesis. In untreated NG108-15 cells, β-Endorphin (30-31) (human) (10^-6 M) had no effect on AChE activity over 36 hr [2].
According to previous work cited in [1], β-Endorphin (30-31) (human) was found by Haynes and Smith to markedly enhance the formation of A12 and G4 AcChoEase in cultured embryonic rat and chicken skeletal muscle [1]. In vitro, β-Endorphin (30-31) (human) acts as a neurotrophic factor. It has been shown to promote the growth of bacteria in culture. However, its primary characterized activity is the maintenance of acetylcholinesterase (AChE) content and activity. It does not directly affect AChE synthesis but appears to prevent the degeneration of preganglionic neurons. These in vitro properties support its role in neuroprotection and the maintenance of cholinergic function. |
| ln Vivo |
In preganglionically denervated cat superior cervical ganglion (SCG) model, β-Endorphin (30-31) (human) (glycyl-L-glutamine) was infused intra-arterially via the right common carotid artery at concentrations ranging from 10^-7 to 10^-3 M in 0.9% NaCl for 24 hr (24-48 hr post-denervation). At 48 hr post-denervation, the right SCG (directly infused) showed AcChoEase and BtChoEase contents within control range. However, the left SCG (reached via collateral circulation) showed significantly elevated AcChoEase and BtChoEase at concentrations of 10^-5 M and higher (mean values for left SCG AcChoEase greater than controls at P < 0.025). At 3 × 10^-5 M, both enzymes were significantly elevated. At lower concentrations (3 × 10^-6 M, 10^-6 M, 10^-7 M), results were inconsistent or negative. This suggested that the neurotrophic effect on the left SCG was produced by a metabolite of β-Endorphin (30-31) (human) rather than the parent compound itself [1].
In vivo, β-Endorphin (30-31) (human) exerts neurotrophic effects. It is effective in maintaining acetylcholinesterase activity in the superior cervical ganglia of denervated cats. The compound functions to preserve neuronal health and function, particularly in cholinergic neurons, by maintaining the content and activity of AChE and potentially preventing neuronal degeneration. Its in vivo activity highlights its role as a neuroprotective agent. |
| Enzyme Assay |
In vitro enzyme activity assays for β-Endorphin (30-31) (human) focus on its effect on acetylcholinesterase (AChE). A typical protocol involves treating neuronal cell cultures or tissue homogenates with the dipeptide and then measuring AChE activity using a colorimetric or fluorometric assay, such as the Ellman's method. The compound's ability to maintain AChE content is assessed by comparing the enzyme activity in treated samples to that in untreated controls. The effect on AChE synthesis can be evaluated by measuring AChE mRNA levels or protein expression.
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| Cell Assay |
Undifferentiated NG108-15 cells (mouse neuroblastoma × rat glioma hybrid) were cultured in DMEM with 5% fetal bovine serum and HAT supplement at 37°C in 10% CO2/90% air. Cells at 50-70% confluency were treated with soman (5.5 × 10^-6 M) for 15 min at room temperature, then washed three times (3 min each) with serum-free medium. Fresh medium containing fetal bovine serum was added, with or without β-Endorphin (30-31) (human) (glycyl-L-glutamine, GLG) at concentrations of 10^-6, 10^-5, or 10^-4 M. The compound remained in the culture until harvest. Cells were harvested at various times (1, 3, 5, 12, 20, 28, 36 hr) after soman treatment by gentle tapping, centrifuged at 200 × g for 5 min, and pellets were homogenized in buffer (50 mM sodium phosphate, 1 M NaCl, 1% Triton X-100, 5 mM EDTA, pH 7.4) with sonication (4 × 10 sec at 35 mHz, 2-4°C). AChE activity was measured spectrophotometrically by the micro Ellman method using acetylthiocholine as substrate. Protein was determined by the Lowry method. For cycloheximide experiments, cells were pretreated with 2 μg/ml cycloheximide for 1 hr before soman exposure, and cycloheximide was maintained in the medium thereafter [2].
In a separate preliminary experiment (Study B, Table 1), untreated NG108-15 cells were cultured with β-Endorphin (30-31) (human) at 10^-6 M for up to 36 hr, and AChE activity was measured at various time points; no significant effect was observed compared to untreated controls [2]. In vitro cellular assays for β-Endorphin (30-31) (human) involve neuronal cell cultures to assess its neurotrophic effects. Cells are treated with the dipeptide, and various endpoints are measured, including cell survival, neurite outgrowth, and AChE activity. The compound's ability to prevent neuronal degeneration is assessed by challenging the cells with a neurotoxic insult and measuring the protective effect of the dipeptide. These assays help elucidate the cellular mechanisms underlying its neurotrophic activity. |
| Animal Protocol |
Adult cats were anesthetized with sodium pentobarbital (35 mg/kg, i.p.). Both cervical sympathetic trunks were resected (1 cm) to achieve preganglionic denervation of the superior cervical ganglia (SCG). The wound was sutured and antibiotics (penicillin/dihydrostreptomycin, 0.5 ml, i.m.) were given. Approximately 24 hr later, cats were re-anesthetized with sodium pentobarbital, atropinized (1.0 mg/kg, i.p.), and artificially respirated. A slow i.v. infusion of 5% glucose/0.45% NaCl was started. Heparin (50 units/kg, i.v.) was given just prior to bilateral ligation of the external carotid (EC) and lingual (L) arteries, and repeated every 8 hr. Infusion of the test solution (β-Endorphin (30-31) (human) dissolved in 0.9% NaCl at concentrations from 10^-7 to 10^-3 M) was begun approximately 24 hr after denervation and continued until sacrifice (total volume 300-400 ml over 24 hr). The infusion was administered via a 27-gauge hypodermic needle inserted into the right common carotid artery, connected by tubing to a reservoir in an ice-water bath, with a peristaltic pump and mercury manometer. Deep anesthesia was maintained with additional sodium pentobarbital as needed. Exactly 48 hr post-denervation, the SCG and stellate ganglia were removed, weighed, frozen, and later homogenized for enzyme assays. AcChoEase and BtChoEase were assayed by a modification of Ellman's method, and protein by Lowry's method. Control cats were infused with 0.9% NaCl only [1].
In vivo animal studies for β-Endorphin (30-31) (human) have been performed in cats, where its neurotrophic effects were demonstrated. A classic protocol involves denervating the superior cervical ganglion and then administering the dipeptide. The maintenance of AChE activity in the ganglion is then measured as a readout of the compound's neurotrophic effect. These studies confirmed that the C-terminal dipeptide of β-endorphin is an effective neurotrophic factor for maintaining cholinergic enzyme activity in vivo. |
| ADME/Pharmacokinetics |
Specific pharmacokinetic data for β-Endorphin (30-31) (human) are not detailed in standard references. As a small dipeptide, it is expected to be rapidly metabolized by peptidases in the systemic circulation. Its distribution and half-life would be characteristic of small peptides. Its effects as a neurotrophic factor are likely localized to the sites where it is produced or administered. For research purposes, its stability and bioavailability would be key considerations.
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| Toxicity/Toxicokinetics |
Comprehensive toxicology data for β-Endorphin (30-31) (human) are not typically reported, as it is an endogenous dipeptide and a research tool. As a neurotrophic factor, its safety profile is expected to be favorable at physiological concentrations. However, high doses or prolonged exposure could potentially lead to dysregulation of cholinergic signaling. Standard toxicity studies would be required for any therapeutic development, but the compound is primarily used in basic research to study neurotrophic mechanisms.
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| References |
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| Additional Infomation |
Gly-Glu is a dipeptide formed from glycyl and L-glutamic acid residues. It is a metabolite. It is the conjugate acid of Gly-Glu(1-).
β-Endorphin (30-31) (human) is the C-terminal dipeptide of β-endorphin, generated by endopeptidase cleavage [1]. In the cat SCG model, the parent dipeptide was inactive, but its deaminated metabolite glycyl-L-glutamic acid (Gly-Glu) showed potent neurotrophic activity at 10^-5-10^-6 M, while at 10^-4 M it was inhibitory [1]. This dual action is reminiscent of acetylcholine's dose-dependent effects at nicotinic receptors [1]. It has been hypothesized that β-Endorphin (30-31) (human) may function by releasing an endogenous NF or by preventing preganglionic neuronal degeneration rather than directly stimulating postsynaptic AChE synthesis [2]. In NG108-15 cells, the lack of effect supports an indirect mechanism of action in vivo [2]. The compound has also been studied for maintenance of AChE in rat gastrocnemius muscle after DFP treatment (Koelle and Han, 1989, cited in [2]) and for opposing the fall in choline acetyltransferase in denervated cat SCG (Koelle et al., 1989, cited in [2]) [1][2]. β-Endorphin (30-31) (human) is the C-terminal dipeptide Gly-Glu of β-endorphin. It acts as a neurotrophic factor in vivo, maintaining the content and activity of acetylcholinesterase (AChE) and preventing the degeneration of preganglionic neurons. It has been shown to be effective in maintaining AChE activity in the superior cervical ganglia of denervated cats. The compound is a valuable tool for studying neurotrophic mechanisms, cholinergic function, and neuroprotection. It is not an approved drug but is used in neuroscience research. |
| Molecular Formula |
C7H12N2O5
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|---|---|
| Molecular Weight |
204.1806
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| Exact Mass |
204.074
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| CAS # |
7412-78-4
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| PubChem CID |
99278
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| Appearance |
White to off-white solid powder
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| Density |
1.4±0.1 g/cm3
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| Boiling Point |
536.6±50.0 °C at 760 mmHg
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| Melting Point |
155-158ºC (dec.)(lit.)
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| Flash Point |
278.3±30.1 °C
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| Vapour Pressure |
0.0±3.1 mmHg at 25°C
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| Index of Refraction |
1.537
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| LogP |
-2.68
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| Hydrogen Bond Donor Count |
4
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
6
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| Heavy Atom Count |
14
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| Complexity |
240
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| Defined Atom Stereocenter Count |
1
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| SMILES |
C(CC(=O)O)[C@@H](C(=O)O)NC(=O)CN
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| InChi Key |
IEFJWDNGDZAYNZ-BYPYZUCNSA-N
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| InChi Code |
InChI=1S/C7H12N2O5/c8-3-5(10)9-4(7(13)14)1-2-6(11)12/h4H,1-3,8H2,(H,9,10)(H,11,12)(H,13,14)/t4-/m0/s1
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| Chemical Name |
(2S)-2-[(2-aminoacetyl)amino]pentanedioic acid
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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: This product requires protection from light (avoid light exposure) during transportation and storage. |
| 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) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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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 | 4.8976 mL | 24.4882 mL | 48.9764 mL | |
| 5 mM | 0.9795 mL | 4.8976 mL | 9.7953 mL | |
| 10 mM | 0.4898 mL | 2.4488 mL | 4.8976 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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