| Size | Price | Stock | Qty |
|---|---|---|---|
| 5mg |
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| 10mg |
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| 25mg |
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| Other Sizes |
| Targets |
A1 adenosine receptor (selective agonist).
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|---|---|
| ln Vitro |
Adenosylamine homologs lessen oxidative damage in cochlea exposed to noise, protecting sensory hair cells. In cochlear tissue, adenosylamine homologs also lessen cisplatin-induced apoptosis, particularly in sensory hair cells and striatal border cells. Adenosylamine homologues have otoprotective properties that block the release of glutamate via presynaptic A1 receptors and voltage-gated Ca2+ channel inhibition, which prevents the activation of the pathways leading to necrotic and apoptotic cell death [1].
In vitro studies demonstrate that ADAC is a selective agonist of the A1 adenosine receptor, a G protein-coupled receptor that plays a crucial role in cellular metabolism and signaling. Activation of A1 adenosine receptors by ADAC modulates various cellular processes including neurotransmitter release, ion channel activity, and cAMP production. The compound has been shown to have neuroprotective effects in various in vitro models of neuronal injury. ADAC's anti-inflammatory activity is mediated through adenosine receptor-dependent pathways that inhibit pro-inflammatory cytokine production and promote tissue protection. The compound also exhibits cardioprotective effects through A1 receptor-mediated preconditioning. |
| ln Vivo |
Treatment with adenosylamine congener (25-300 μg/kg/day; i.p.; daily; for 5 days; male Wistar rats) is most effective in the first 24 hours following noise exposure at dosages >50 μg/kg; it offers protection of up to 21 dB. Adenosylamine congeners have a dose- and time-dependent effect on mitigating noise-induced hearing loss [1].
In vivo studies have demonstrated that ADAC ameliorates noise-induced and cisplatin-induced cochlear injury by activating A1 adenosine receptors, which protects against cochlear damage caused by excessive noise exposure or cisplatin administration. The compound exhibits neuroprotective effects in various animal models of neurological injury, including ischemia and neurodegenerative conditions. ADAC's anti-inflammatory and cardioprotective activities have also been demonstrated in vivo, where it reduces inflammation and protects cardiac tissue from ischemic damage. These findings support the therapeutic potential of A1 adenosine receptor agonists for treating hearing loss, neurodegenerative diseases, and cardiovascular conditions. |
| Enzyme Assay |
For receptor binding assays, competitive binding studies are performed using membrane preparations from cells or tissues expressing the A1 adenosine receptor. Membranes are incubated with a radiolabeled A1 receptor ligand (e.g., [3H]-DPCPX) and varying concentrations of ADAC. Bound radioactivity is separated by filtration and measured by scintillation counting. Binding affinity (Ki) is calculated from competition curves by non-linear regression analysis. Receptor activation is assessed using functional assays measuring A1 receptor-mediated inhibition of adenylyl cyclase activity or cAMP accumulation in cells expressing the receptor. EC50 values are determined from dose-response curves.
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| Cell Assay |
Cellular assays for ADAC typically involve culturing cells that endogenously or recombinantly express A1 adenosine receptors (e.g., neurons, cardiomyocytes, or CHO cells). Cells are treated with ADAC at various concentrations, and receptor activation is assessed by measuring downstream signaling events such as inhibition of cAMP accumulation (using ELISA or HTRF-based cAMP assays), activation of G protein-coupled inwardly rectifying potassium channels (GIRK), or inhibition of calcium channels. Neuroprotective effects are evaluated in models of neuronal injury such as glutamate excitotoxicity or oxidative stress. Anti-inflammatory effects are assessed by measuring cytokine production in activated immune cells.
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| Animal Protocol |
Animal/Disease Models: Male Wistar rats (8-10 weeks old) received noise exposure treatment [1]
Doses: 25 μg/kg/day, 50 μg/kg/day, 100 μg/kg/day, 200 μg/kg/day , 300 μg/kg/day Doses: intraperitoneal (ip) injection; daily; for 5 days Experimental Results: Most effective in the first 24 hrs (hrs (hours)) after noise exposure at doses >50 μg/kg and provided up to 21 dB of protection (8- average over the 28 kHz range). In vivo efficacy of ADAC is evaluated in various animal models depending on the therapeutic indication. For cochlear injury studies, rodents are exposed to noise or treated with cisplatin to induce hearing loss, and then treated with ADAC via intraperitoneal or intravenous administration. Hearing function is assessed by auditory brainstem response (ABR) measurements, and cochlear morphology is examined by histology. For neuroprotection studies, animal models of ischemia, traumatic brain injury, or neurodegenerative disease are used, with endpoints including neurological deficit scoring, infarct volume measurement, and histopathological assessment. Cardioprotective effects are evaluated in models of myocardial ischemia-reperfusion injury. |
| ADME/Pharmacokinetics |
Pharmacokinetic properties of ADAC have been characterized in preclinical studies. As an adenosine derivative, the compound is expected to have a short half-life due to rapid metabolism and uptake by cells. The compound's molecular weight of 576.6 and polar nature influence its absorption, distribution, metabolism, and excretion (ADME) properties. Key PK parameters including half-life, clearance, volume of distribution, and bioavailability are determined using LC-MS/MS or HPLC analysis of plasma and tissue samples following administration. The compound's ability to penetrate the blood-brain barrier is important for its neuroprotective applications.
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| Toxicity/Toxicokinetics |
Toxicological evaluation of ADAC is typically conducted in parallel with efficacy studies in animal models. Standard toxicology assessments include acute toxicity studies to determine the maximum tolerated dose, observation of clinical signs and physiological parameters, and histopathological examination of major organs following repeated dosing. As an adenosine receptor agonist, potential cardiovascular effects such as changes in heart rate and blood pressure are carefully monitored. The compound's safety profile is established to define the therapeutic window for research applications. The compound is intended for laboratory research use only and is not approved for clinical administration.
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| References | |
| Additional Infomation |
ADAC is a research tool compound used for studying adenosine receptor signaling and its role in neuroprotection, cochlear protection, cardioprotection, and inflammation. The compound is not approved for clinical use and is intended for laboratory research purposes only. Its mechanism of action involves selective activation of the A1 adenosine receptor, which triggers downstream signaling pathways including inhibition of adenylyl cyclase, activation of G protein-coupled inwardly rectifying potassium channels, and modulation of neurotransmitter release. These signaling events contribute to the compound's neuroprotective, anti-inflammatory, and cardioprotective effects. ADAC is valuable for investigating the therapeutic potential of A1 adenosine receptor agonists in various pathological conditions.
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| Molecular Formula |
C28H32N8O6.H2O
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|---|---|
| Molecular Weight |
594.61896
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| Exact Mass |
576.244
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| Elemental Analysis |
C, 58.32; H, 5.59; N, 19.43; O, 16.65
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| CAS # |
96760-69-9
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| PubChem CID |
126054
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| Appearance |
Solid powder
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| LogP |
1.217
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| Hydrogen Bond Donor Count |
7
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| Hydrogen Bond Acceptor Count |
11
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| Rotatable Bond Count |
11
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| Heavy Atom Count |
42
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| Complexity |
887
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| Defined Atom Stereocenter Count |
4
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| SMILES |
OC[C@@H]1[C@H]([C@H]([C@H](N2C=NC3=C(N=CN=C32)NC4=CC=C(CC(NC5=CC=C(CC(NCCN)=O)C=C5)=O)C=C4)O1)O)O
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| InChi Key |
JFRJCQJVFMHZOO-QZHHGCDDSA-N
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| InChi Code |
InChI=1S/C28H32N8O6/c29-9-10-30-21(38)11-16-1-5-18(6-2-16)34-22(39)12-17-3-7-19(8-4-17)35-26-23-27(32-14-31-26)36(15-33-23)28-25(41)24(40)20(13-37)42-28/h1-8,14-15,20,24-25,28,37,40-41H,9-13,29H2,(H,30,38)(H,34,39)(H,31,32,35)/t20-,24-,25-,28-/m1/s1
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| Chemical Name |
N-(2-aminoethyl)-2-[4-[[2-[4-[[9-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]purin-6-yl]amino]phenyl]acetyl]amino]phenyl]acetamide
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| Synonyms |
Adenosine amine congener; 6-Adac; ADAC.
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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 |
| 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 : ~31.25 mg/mL (~54.20 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (3.61 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.08 mg/mL (3.61 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. 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. View More
Solubility in Formulation 3: ≥ 2.08 mg/mL (3.61 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.6817 mL | 8.4087 mL | 16.8175 mL | |
| 5 mM | 0.3363 mL | 1.6817 mL | 3.3635 mL | |
| 10 mM | 0.1682 mL | 0.8409 mL | 1.6817 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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