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Related Concept Videos

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Agonists can bind with and activate receptors, resulting in the formation of drug-receptor complexes. Once formed, these complexes catalyze many biochemical processes at the cellular level and subsequently induce a pharmacologic response. The degree of response is directly proportional to the fraction of activated receptors, which in turn, depends on the concentration of the drug at the receptor site as well as the sensitivity of the receptor. An increase in the administered dose contributes to...
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The potency of a drug is the measure of its ability to produce a biological response and can be compared by looking at the half-maximum effective concentration or EC50 values of different drugs. A lower EC50 value indicates higher potency of the drug. In the dose–response curve of two antihypertensive drugs, candesartan and irbesartan, a significant difference is observed in their EC50 values. A lower EC50 value for candesartan indicates that it is more potent than irbesartan, as it...
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Drugs exert their therapeutic effects by interacting with receptors, enzymes, or ion channels that are present throughout the human body. The strength and duration of the interaction between a drug and its target receptor are characterized by the selectivity and specificity of the drug. Selectivity refers to a drug's strong preference for its intended target over other targets. For instance, isoprenaline, a non-selective β-adrenergic agonist, interacts with both β1- and...
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Self-esteem—an individual's overall evaluation of their worth—plays a complex role in psychological functioning and well-being. It is often associated with many positive traits, such as confidence, optimism, and perseverance. Individuals with high self-esteem typically experience better sleep, manage peer pressure more effectively, and report greater life satisfaction. Conversely, low self-esteem has been consistently linked with increased risks of depression, anxiety, and poor...
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Lesson: Translation
Translation is the process of synthesizing proteins from the genetic information carried by messenger RNA (mRNA). Following transcription, it constitutes the final step in the expression of genes. This process is carried out by ribosomes, complexes of protein and specialized RNA molecules. Ribosomes, transfer RNA (tRNA), and other proteins produce a chain of amino acids—the polypeptide—as the end product of translation.
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Initiating translation is complex because it involves multiple molecules. Initiator tRNA, ribosomal subunits, and eukaryotic initiation factors (eIFs) are all required to assemble on the initiation codon of mRNA. This process consists of several steps that are mediated by different eIFs.
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Assessment and Evaluation of the High Risk Neonate: The NICU Network Neurobehavioral Scale
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Translating the dose response into risk and benefit.

John B Warren1

  • 1Flat 15, Porters Edge, 29 Surrey Quays Road, London, SE16 7FZ, UK.

British Journal of Clinical Pharmacology
|April 5, 2019
PubMed
Summary
This summary is machine-generated.

Optimizing medication requires balancing drug benefit against harm by matching the drug to the individual and dose. Understanding the dose-response relationship, including the effective dose 50 (ED50), is crucial for rational drug dosing.

Keywords:
EMAFDAPhase 1-3clinical trialsmortalitysafety

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Area of Science:

  • Pharmacology
  • Clinical Pharmacology
  • Drug Safety

Background:

  • Choosing medication involves balancing benefits and harms (risk-benefit).
  • Rational drug dosing relies on understanding the dose-response relationship and the effective dose 50 (ED50).
  • ED50 is used to measure both drug efficacy and safety, with efficacy quantification being more straightforward than safety assessment.

Purpose of the Study:

  • To review the translation of in vitro dose-response curves into clinical, dose-dependent risk-benefit assessments.
  • To discuss the limitations in optimizing individual risk-benefit ratios and the consideration of no-drug options.
  • To highlight the importance of defining these limitations for patient education on treatment dose options.

Main Methods:

  • Review of clinical trial data to assess dose-dependent risk-benefit.
  • Analysis of dose-response curves for drug efficacy and safety.
  • Discussion of limitations in current knowledge regarding optimal dosing.

Main Results:

  • Efficacy quantification is generally straightforward (e.g., blood pressure reduction, decreased cardiovascular events).
  • Safety assessment is more complex, often involving subjective evaluation of adverse events.
  • Translating in vitro data to clinical risk-benefit requires careful consideration of trial data.

Conclusions:

  • Defining a science-based therapeutic window is reassuring but requires translation into clinical practice.
  • Limitations exist in optimizing individual drug dosing for risk-benefit.
  • Clear communication of pharmacological rationale and dose options is essential for patient education.