Capadenoson

SKU: orb1296185

Description

Capadenoson (BAY 68-4986) is a potent and selective agonist for the adenosine A1 receptor. This compound is utilized in cardiovascular and metabolic research, with studies investigating its effects in both in vitro assays and in vivo models of ischemia and heart failure.

Research Area

Neuroscience, Pharmacology & Drug Discovery

Key Properties

• CAS Number: 544417-40-5
• MW: 520.03
• Purity: 99.62% (May vary between batches)
• Formula: C₂₅H₁₈ClN₅O₂S₂
• SMILES: Nc1nc(SCc2csc(n2)-c2ccc(Cl)cc2)c(C#N)c(-c2ccc(OCCO)cc2)c1C#N
• Target: Adenosine Receptor
• Solubility: DMSO:70 mg/mL (134.61 mM);H2O:Insoluble;10% DMSO+90% Corn Oil:3.3 mg/mL (6.35 mM)

Bioactivity

• In Vivo:
  In vivo experiments involving Wistar rats and SHR showed that pre-treatment with Capadenoson (0.15 mg/kg) for 5 days led to a consistent plasma concentration of the drug, averaging 7.63 μg/L on days 4 and 5. This level remained stable even after a 2-hour physical restraint stress test performed on day 5, administered 3 hours post Capadenoson intake, indicating steady absorption and efficacy throughout the pre-test period.
• In Vitro:
  To elucidate the pharmacological effects of Capadenson, GTP shift assays compare its action to the A1-agonist CCPA and A1-antagonist DPCPX on rat cortical brain membranes. CCPA has a Ki value of 4.2 nM, which increases to 64 nM with 1 mM GTP, demonstrating a GTP shift of 15. Conversely, DPCPX displays a GTP shift of 1, indicating nearly unchanged Ki values with and without GTP. Capadenson presents a Ki value of 24 nM, escalating to 116 nM when exposed to 1 mM GTP, equating to a GTP shift of 5. This data highlights the distinct interactions of these compounds with GTP and their varied pharmacological profiles.
• Animal Research:
  A total of 14 Wistar rats and 18 SHR (bodyweight 200-50 g, all-female) underwent experiments to evaluate the exocytotic, stimulation-induced NE release during electrical field stimulation. Rats are killed by an injection of pentobarbital i.p. (0.5 mL/100 mg body weight), and hearts are rapidly excised, and placed in ice-cold Krebs-Henseleit solution (KHL). They are quickly mounted on a Langendorff apparatus for retrograde perfusion with KHL. Perfusion rate is kept constant at 10 mL/min, the temperature is adjusted to 37°C, and the pH to 7.4 through bubbling with 5% CO2/95% O2. Via an inflow line desipramine at a concentration of 10 7 M is added to the perfusion buffer. After an equilibration period of 20 minutes, electrical field stimulation is commenced via two metal paddles adjacent to both sides of the beating heart for 1 minute (5V, 6 Hz). We collected the efflux in plastic tubes the minute before, during, and 3 minutes after the stimulation. These are rapidly frozen in liquid nitrogen and stored at 20°C till analysis. The NE release is calculated as the cumulative release induced by electrical stimulation. After the first stimulation (S1), the study drug Capadenoson at concentrations of 30 μg/L (6×10^ 8 M) or 300 μg/L(6×10^ 7 M), or CCPA (10^ 6 M), respectively, are added via separate perfusion lines for 30 minutes. After this time a second stimulation (S2) is executed to determine the effect of the drugs on NE release compared to the first stimulation. The effect of each pharmacological intervention is analyzed by calculating the ratio of NE release induced by the second and first stimulation (S2/S1 ratio).

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

A1, AdenosineReceptor, Adenosine Receptor, Capadenoson, BAY 68-4986, P1 receptor, inhibit, Inhibitor

Compound Identifiers

PubChem CID

9936489