ArticleMolecules (Basel, Switzerland)2024
Selectivity Studies and Free Energy Calculations of AKT Inhibitors.
Article in Molecules (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Synthesis, Structural Characterization, and Investigation of Biological Effects of Novel Benzothiazole-Triazole Derivatives Designed as AKT Kinase Inhibitors.Chemical biology & drug design · 2026Article
- Rational Design of a Novel Anti-Cancer Hybrid Peptide Inhibiting the PI3K/AKT and CDK2 Signaling Pathways using Molecular Dynamics Simulations.Probiotics and antimicrobial proteins · 2026Article
- Optimizing Component Formula Extracted from Ginseng and Salvia Inhibits Lung Cancer Metastasis and EMT via Suppressing AKT/GSK-3β/β-catenin Pathway.Journal of ginseng research · 2026Article
- Honey Lemon Alleviates Alcoholic Liver Disease via Multi-Target Synergistic Mechanisms: An Integrated Study of Network Pharmacology, Molecular Docking, and Animal Experiments.Foods (Basel, Switzerland) · 2026Article
- Exploring sesquiterpene lactone as a dual therapeutic agent for diabetes and oxidative stress: insights into PI3K/AKT modulation.3 Biotech · 2024Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein kinase B (PKB) or AKT protein is an important target for cancer treatment. Significant advances have been made in developing ATP-competitive inhibitors and allosteric binders targeting AKT1. However, adverse effects or toxicities have been found, and the cutaneous toxicity was found to be linked to the inhibition of AKT2. Thus, selective inhibition of AKT inhibitors is of significance. Our work, using the Schrödinger Covalent Dock (CovDock) program and the Movable Type (MT)-based free energy calculation (ΔG), yielded small mean errors for the experimentally derived binding free energy (ΔG). The docking data suggested that AKT1 binding may require residues Asn54, Trp80, Tyr272, Asp274, and Asp292, whereas AKT2 binding would expect residues Phe163 and Glu279, and AKT3 binding would favor residues Glu17, Trp79, Phe306, and Glu295. These findings may help guide AKT1-selective or AKT3-selective molecular design while sparing the inhibition of AKT2 to minimize the cutaneous toxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.