| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| Targets |
Antide acetate exerts its effects by binding to the gonadotropin-releasing hormone receptor (GnRHR) in the anterior pituitary. As a GnRH antagonist, it competes with endogenous neurohormone GnRH (LHRH) for binding to its receptor. By blocking the GnRH receptor, antide acetate prevents the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary gland. This suppression of gonadotropin release leads to reduced gonadal steroid production. The compound's sequence is Ac-D-2Nal-D-Phe(4-Cl)-D-3Pal-Ser-Lys(nicotinoyl)-D-Lys(nicotinoyl)-Leu-Lys(iPr)-Pro-D-Ala-NH2·CH3CO2H. Antide shows negligible histamine release compared to other GnRH antagonists.
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| ln Vitro |
In vitro, antide acetate has been shown to effectively antagonize GnRH receptor activation. The compound binds to the GnRH receptor with high affinity, preventing GnRH-induced downstream signaling. In pituitary cell cultures, antide acetate inhibits GnRH-stimulated LH and FSH secretion in a dose-dependent manner. The compound's antagonistic activity is characterized by its ability to compete with radiolabeled GnRH or GnRH agonists for receptor binding. Antide acetate's high antiovulatory activity has been demonstrated in various in vitro models. The compound's negligible histamine release profile makes it advantageous over other GnRH antagonists that may cause histamine-related side effects. Receptor binding affinity and selectivity can be assessed using competitive binding assays with pituitary membrane preparations.
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| ln Vivo |
Antipeptides (subcutaneous injection; 1, 3, 6, 10, and 15 mg/kg; once or for 5 consecutive days) induce long-term chemical castration in adult male rats and cynomolgus monkeys [1].
In vivo, antide acetate has been extensively studied for its effects on the hypothalamic-pituitary-gonadal axis. Administration of antide acetate results in suppression of LH and FSH release from the pituitary gland in animal models. The compound shows high antiovulatory activity in female animals. Studies have evaluated the direct in vivo effects of GnRH antagonists, including antide, on ovarian follicular development in prepubertal eCG-treated rats. GnRH analogs, including agonists and antagonists, are widely used to inhibit gonadotropin pituitary release. Antide acetate's effects on the pituitary-gonadal axis have been studied in various species, demonstrating its efficacy as a GnRH receptor antagonist. The compound's negligible histamine release in vivo supports its favorable safety profile. |
| Enzyme Assay |
For in vitro receptor binding assays, antide acetate is evaluated using cell-free systems to assess its affinity for the GnRH receptor. Radioligand binding assays are performed using membrane preparations from cells expressing GnRH receptors, typically from pituitary tissue or recombinant expression systems. Competitive binding experiments with radiolabeled GnRH or specific agonists allow determination of Ki and IC50 values. Scatchard analysis is used to calculate receptor binding affinity. Binding specificity is assessed using receptor-selective ligands. These cell-free assays help characterize antide acetate's receptor binding profile and identify the molecular determinants of receptor recognition and antagonism.
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| Cell Assay |
In vitro cellular assays for antide acetate are performed using pituitary cells or cell lines expressing GnRH receptors. Primary pituitary cell cultures are commonly used to assess the compound's effects on hormone secretion. Cells are cultured in appropriate media and treated with antide acetate at various concentrations, with or without GnRH stimulation. LH and FSH secretion into the culture medium is measured using ELISA or radioimmunoassay. Receptor activation can also be assessed by measuring downstream signaling events such as calcium mobilization, MAPK activation, or inositol phosphate production. Cell viability and cytotoxicity assays may be performed to assess compound safety. The potency of antagonism is determined by the ability to inhibit GnRH-stimulated hormone release.
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| Animal Protocol |
Animal/Disease Models: cynomolgus monkey and rat [1]
Doses: 1, 3, 6, 10 and 15 mg/kg Route of Administration: subcutaneous injection, once or for 5 days Experimental Results: Dose-dependent inhibition of serum LH concentration (rats only) and testosterone and testicular, prostate, and seminal vesicle weights. Long-lasting castration-like effects were achieved in rats over a concentration range of 6 (less than or equal to 8 weeks) to 15 mg/kg (greater than 8 weeks). Long-term inhibition was induced at a dose of only 15 mg/kg and lasted only 2-3 weeks in cynomolgus monkeys. In vivo animal experiments with antide acetate are conducted to study its effects on reproductive function. Rodent models are commonly used, including prepubertal eCG-treated rats for ovarian follicular development studies. Antide acetate is administered via subcutaneous or intraperitoneal injection at various doses. Hormone levels (LH, FSH, estradiol, testosterone, progesterone) are measured in blood samples using immunoassays. Ovarian or testicular tissues are harvested for histological analysis of follicular development, spermatogenesis, or steroidogenesis. Fertility studies may be conducted to assess antiovulatory activity. Ovulation rates are determined by counting oocytes in the oviducts. Histamine release can be monitored as a safety parameter. |
| ADME/Pharmacokinetics |
Pharmacokinetic properties of antide acetate are characteristic of peptide therapeutics. The compound has a molecular weight of 1651.34. As a peptide, antide acetate is not orally bioavailable and is typically administered via injection. The compound should be stored as a powder at -20°C for up to 3 years and in solution at -80°C for up to 1 year. Detailed PK parameters such as half-life, Cmax, Tmax, AUC, and protein binding are not extensively documented in the available literature. The compound's stability may be influenced by temperature and light exposure. For in vivo studies, antide acetate is typically formulated in appropriate vehicles for parenteral administration. Researchers should follow standard protocols for peptide handling and storage.
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| Toxicity/Toxicokinetics |
The toxicological profile of antide acetate is not extensively characterized in the literature. The compound is known to release negligible histamine, which is a favorable safety feature compared to some other GnRH antagonists. However, comprehensive toxicity studies including acute, subchronic, and chronic toxicity assessments are limited. As a GnRH antagonist, antide acetate may cause reversible suppression of gonadal function, which is the intended pharmacological effect in some research contexts. The compound is strictly intended for research use only and not for human therapeutic applications without appropriate regulatory approval. Researchers should follow standard laboratory safety practices when handling antide acetate.
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| References | |
| Additional Infomation |
Antide acetate is a valuable research tool for studying the hypothalamic-pituitary-gonadal axis and reproductive hormone regulation. The compound is used to investigate the mechanisms of GnRH receptor signaling and the physiological roles of LH and FSH. It is also relevant for research into prostate cancer, as GnRH antagonists are used in prostate cancer therapy. Antide acetate's negligible histamine release profile makes it useful for comparative studies with other GnRH antagonists. The compound can be employed to study the direct effects of GnRH antagonists on ovarian and testicular function, independent of their effects on pituitary gonadotropin secretion. It is also valuable for research into reproductive disorders and contraception.
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| Molecular Formula |
C82H108N17O14CL
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|---|---|
| Molecular Weight |
1591.29342
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| Exact Mass |
1589.795
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| CAS # |
112568-12-4
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| PubChem CID |
16130938
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| Appearance |
White to off-white solid powder
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| Density |
1.3±0.1 g/cm3
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| Boiling Point |
1798.0±65.0 °C at 760 mmHg
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| Flash Point |
1041.2±34.3 °C
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| Vapour Pressure |
0.0±0.3 mmHg at 25°C
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| Index of Refraction |
1.593
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| LogP |
4.91
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| Hydrogen Bond Donor Count |
14
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| Hydrogen Bond Acceptor Count |
18
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| Rotatable Bond Count |
46
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| Heavy Atom Count |
114
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| Complexity |
3110
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| Defined Atom Stereocenter Count |
10
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| SMILES |
ClC1=CC=C(C=C1)C[C@H](C(N[C@H](CC1=CN=CC=C1)C(N[C@@H](CO)C(N[C@@H](CCCCNC(C1=CN=CC=C1)=O)C(N[C@H](CCCCNC(C1=CN=CC=C1)=O)C(N[C@@H](CC(C)C)C(N[C@@H](CCCCNC(C)C)C(N1CCC[C@H]1C(N[C@@H](C(N)=O)C)=O)=O)=O)=O)=O)=O)=O)=O)NC([C@@H](CC1C=CC2=CC=CC=C2C=1)NC(C)=O)=O
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| InChi Key |
QRYFGTULTGLGHU-NBERXCRTSA-N
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| InChi Code |
InChI=1S/C82H108ClN17O14/c1-50(2)41-65(76(108)95-64(26-11-12-37-88-51(3)4)82(114)100-40-18-27-70(100)81(113)91-52(5)71(84)103)96-75(107)63(25-10-14-39-90-73(105)60-23-17-36-87-48-60)93-74(106)62(24-9-13-38-89-72(104)59-22-16-35-86-47-59)94-80(112)69(49-101)99-79(111)68(45-56-19-15-34-85-46-56)98-78(110)67(43-54-29-32-61(83)33-30-54)97-77(109)66(92-53(6)102)44-55-28-31-57-20-7-8-21-58(57)42-55/h7-8,15-17,19-23,28-36,42,46-48,50-52,62-70,88,101H,9-14,18,24-27,37-41,43-45,49H2,1-6H3,(H2,84,103)(H,89,104)(H,90,105)(H,91,113)(H,92,102)(H,93,106)(H,94,112)(H,95,108)(H,96,107)(H,97,109)(H,98,110)(H,99,111)/t52-,62+,63-,64+,65+,66-,67-,68-,69+,70+/m1/s1
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| Chemical Name |
N-[(5R)-5-[[(2S)-2-[[(2S)-2-[[(2R)-2-[[(2R)-2-[[(2R)-2-acetamido-3-naphthalen-2-ylpropanoyl]amino]-3-(4-chlorophenyl)propanoyl]amino]-3-pyridin-3-ylpropanoyl]amino]-3-hydroxypropanoyl]amino]-6-(pyridine-3-carbonylamino)hexanoyl]amino]-6-[[(2S)-1-[[(2S)-1-[(2S)-2-[[(2R)-1-amino-1-oxopropan-2-yl]carbamoyl]pyrrolidin-1-yl]-1-oxo-6-(propan-2-ylamino)hexan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-6-oxohexyl]pyridine-3-carboxamide
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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: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
| 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) |
H2O : ~10 mg/mL (~6.28 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 | 0.6284 mL | 3.1421 mL | 6.2842 mL | |
| 5 mM | 0.1257 mL | 0.6284 mL | 1.2568 mL | |
| 10 mM | 0.0628 mL | 0.3142 mL | 0.6284 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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