Levosemotiadil
Levosemotiadil, an S-isomer of semotiadil, exhibits stronger binding affinity to human serum albumin (HSA) compared to its R-isomer counterpart. This study utilized high-performance frontal analysis (HPFA) to demonstrate that levosemotiadil binds approximately three times more strongly to HSA than semotiadil. The binding parameters were evaluated using Scatchard analysis, revealing specific interactions with the diazepam binding site on HSA. The presence of diazepam decreased the binding affinity of both enantiomers, while warfarin did not alter their binding characteristics. These findings highlight levosemotiadil's potential as a Ca- and Na-channel blocker with significant binding preferences for HSA, crucial for understanding its pharmacokinetics and therapeutic effects.
For research use only. We do not sell to patients.
- CAS No.: 116476-16-5
- Formula: C29H32N2O6S
- Molecular Weight:536.64
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Calcium Channel Isoforms
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Biological Activity
Description
Chemical Information
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CAS No. 116476-16-5
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Molecular Weight 536.64
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Formula C29H32N2O6S
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SMILES
CN(CCOC1=CC=C(OCO2)C2=C1)CCCOC3=C([C@@H]4SC5=CC=CC=C5N(C4=O)C)C=C(C=C3)OC
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Protocol for Pharmacokinetic Study
Pharmacokinetic studies quantify how an organism handles a drug over time through absorption, distribution, metabolism, and excretion, and the core experimental readout is the concentration-time profile of parent drug and, when relevant, metabolites in biological matrices such as plasma, whole blood, urine, bile, or tissue. Pharmacokinetic analysis links dose, route, exposure, clearance, half-life, distribution, bioavailability, and systemic exposure to drug efficacy and toxicity hypotheses rather than measuring a signaling pathway directly. The literature links pharmacokinetics to drug-development phenotypes by showing that drug metabolism and pharmacokinetics influence compound progression, exposure-response interpretation, safety margins, dosing strategy, and failure risk during discovery and development. DMPK science contributes to compound optimization by integrating physicochemical properties, in vitro metabolism, transporter behavior, in vivo exposure, and pharmacodynamic contex
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)