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Related Concept Videos

Drugs that Destabilize Microtubules01:10

Drugs that Destabilize Microtubules

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Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
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Microtubules are dynamic structures that undergo cycles of catastrophe and rescue. The microtubules play a central role in cell division by forming the spindle apparatus for segregating the chromosomes. This makes them ideal targets for regulating dividing cells in tumors and malignant cancer cells. Microtubule stabilizing drugs help stabilize the microtubule formation and promote its polymerization. Paclitaxel was the first microtubule stabilizing agent used as anticancer drug in chemotherapy...
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Pharmacogenomics: Identification of New Drug Targets01:29

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Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...
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Inhibition of Cdk Activity02:34

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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
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Combined Effects of Drugs: Synergism01:27

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Synergism is a useful mechanism where combining two or more drugs is more effective than each constituent used alone. Such combinations are also called supra-additive interactions. The drugs collectively enhance the final therapeutic effect by acting on different targets. Another advantage is that the low dose of each constituent drug is sufficient to achieve the desired effect. This helps reduce the duration of therapy and lower the adverse effects of these drugs.
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Recent Developments on Phenstatins as Potent Antimitotic Agents.

Xing Chen1, Shi-Meng Wang1, Gajjela Bharath Kumar1

  • 1Department of Pharmaceutical Engineering, School of Chemistry, Chemical Engineering and Life Science, Wuhan University of Technology, 205 Luoshi Road, Wuhan, 430070, China.

Current Medicinal Chemistry
|November 8, 2017
PubMed
Summary
This summary is machine-generated.

Phenstatin derivatives show strong antiproliferative and antimitotic effects by inhibiting tubulin polymerization. These compounds are promising anticancer agents, with ongoing clinical evaluations for vascular targeting and antiangiogenic properties.

Keywords:
Antimitotic activityColchicine binding siteCytotoxic activityStructure-activity relationshipTubulin polymerization inhibitionphenstatins.

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Area of Science:

  • Medicinal Chemistry
  • Pharmacology
  • Cancer Biology

Background:

  • Phenstatins and their derivatives exhibit significant antiproliferative activity in preclinical cancer models.
  • Their structural simplicity and stability facilitate the development of potent antimitotic and cytotoxic agents.

Purpose of the Study:

  • To review the literature on phenstatin derivatives' mechanisms of action.
  • To discuss their role as tubulin polymerization inhibitors and cell cycle arrest agents.
  • To highlight their clinical evaluation as vascular targeting agents and their antiangiogenic properties.

Main Methods:

  • A systematic literature search of peer-reviewed research was conducted.
  • The review focused on a specific research question with defined inclusion/exclusion criteria.

Main Results:

  • Phenstatin derivatives inhibit tubulin polymerization by binding to the colchicine site on microtubules.
  • They induce cell cycle arrest at the G2/M phase.
  • Clinical evaluations are underway for their use as vascular targeting/disrupting agents and their direct antiangiogenic effects.

Conclusions:

  • This review discusses the synthesis and structure-activity relationships of phenstatin analogues.
  • Modifications to ring A, ring B, and the keto position are analyzed.
  • The findings provide insights into the medicinal chemistry of phenstatin derivatives for anticancer drug development.