プロフィール詳細

プロジェクトを作成

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Dr. KANIKA V.に依頼

India

In silico drug discovery specialist with expertise in virtual screening using different tools in bioinformatics research

プロフィール概要

Dr. Kanika Verma is a computational biologist with a focus on bioinformatics and drug discovery. In order to find lead molecules and repurpose current medications, she has worked on phytochemical therapeutics, cancer, neurodegeneration, and malaria using virtual screening, molecular dynamics, and systems pharmacology. Prominent research includes the mechanistic investigation of phytochemical-mediated neuroprotective action using Caenorhabditis elegans and neuronal cell lines, the in silico identification of antimalarial leads against multiple biomarkers, and drug repurposing pipelines for breast cancer. Her interdisciplinary, high-impact work has received over 200+ citations and an h-index of 10. Through Kolabtree with deliverables, reproducible data flow, and good documentation end-points, Dr. Verma can offer her clients expertise in computational drug discovery, bioinformatics, phytochemical analysis, and scientific writing. She provides deep domain knowledge, analytical skills, and client-focused programming to translate challenging biological issues into insightful, publishable outcomes.

専門分野

• ☆ Bioinformatics
• ☆ Structural Bioinformatics
• ☆ Neurology
• ☆ Alzheimer's Disease
• ☆ Women's Health
• ☆ Breast Cancer
• ☆ Ovarian Cancer
• ☆ Infectious Disease
• ☆ Tropical Medicine
• ☆ Malaria
• ☆ Pulmonology/Respiratory Disease
• ☆ Lung Cancer
• ☆ Public Health
• ☆ Global Health
• ☆ Cancer Research

サービス

• Writing
• Research
• Consulting

Writing Medical Writing

Research Scientific and Technical Research, Systematic Literature Review

Consulting Scientific and Technical Consulting

職務経験

Scientist B

ICMR-National Institute of Research in Tribal Health

9月 2020 - 現在

Postdoctoral Fellow

Chulalongkorn University

4月 2018 - 3月 2020

学歴

PhD

VIT University

2月 2014 - 9月 2017

MSc.

VIT University

7月 2011 - 7月 2013

BSc

Dayanand Girls College, CSJM University

7月 2008 - 9月 2011

認定資格

• Technical Writing

  Chulalongkorn University

  1月 2025 - 1月 2025

出版物

JOURNAL ARTICLE

Kanika Verma, Panupong Mahalapbutr, Utid Suriya, Tuanjai Somboon, Thitinan Aiebchun, Liyi Shi, Phornphimon Maitarad, Thanyada Rungrotmongkol(2021). In Silico Screening of DNA Gyrase B Potent Flavonoids for the Treatment of Clostridium difficile Infection from PhytoHub Database . Brazilian Archives of Biology and Technology. 64. {FapUNIFESP} ({SciELO})

Kanika Verma and Panupong Mahalapbutr and Atima Auepattanapong and Onnicha Khaikate and Chutima Kuhakarn and Kaito Takahashi and Thanyada Rungrotmongkol (2020). Molecular dynamics simulations of sulfone derivatives in complex with DNA topoisomerase IIα ATPase domain . Journal of Biomolecular Structure and Dynamics. 0. (0). Microsoft.AspNetCore.Mvc.Localization.LocalizedHtmlString 1-10. Taylor & Francis

An Integrative Drug Repurposing Pipeline: Switching Viral Drugs to Breast Cancer @article{https://doi.org/10.1002/jcb.25799, author= {Karuppasamy, Ramanathan and Verma, Kanika and Sequeira, Velin Marita and Basavanna, Lokapriya Nandan and Veerappapillai, Shanthi}, title= {An Integrative Drug Repurposing Pipeline: Switching Viral Drugs to Breast Cancer}, journal= {Journal of Cellular Biochemistry}, volume= {118}, number= {6}, pages= {1412-1422}, keywords= {DRUG-REPURPOSING, BREAST CANCER, ANTI-VIRAL DRUGS, PACLITAXEL}, doi= {https://doi.org/10.1002/jcb.25799}, url= {https://onlinelibrary.wiley.com/doi/abs/10.1002/jcb.25799}, eprint= {https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcb.25799}, abstract= {ABSTRACT The growing incidence rate of breast cancer, coupled with cellular chemotherapeutic resistance, has made this disease one of the most prevalent cancers among women worldwide. Despite the recent efforts to understand the underlying cause of the resistance due to mutation, there are no feasible tactics to overcome this bottleneck. This issue could be addressed by the concept of polypharmacology-disguising drugs present in the pharmacopeia for novel purposes (drug repurposing). Of note, we have proposed a multi-modal computational drug-repositioning stratagem to predict drugs possessing anti-proliferative effect. Our results suggest that Ombitasvir, a Hepatitis C NS5B polymerase inhibitor, could be “repurposed” for the control and prevention of beta-tubulin-driven breast cancers. J. Cell. Biochem. 118: 1412–1422, 2017. © 2016 Wiley Periodicals, Inc.}, year= {2017}} . Journal of Cellular Biochemistry.

Exploring β-Tubulin Inhibitors from Plant Origin using Computational Approach @article{https://doi.org/10.1002/pca.2665, author= {Verma, Kanika and Kannan, Kaavya and V, Shanthi and R, Sethumadhavan and V, Karthick and K, Ramanathan}, title= {Exploring β-Tubulin Inhibitors from Plant Origin using Computational Approach}, journal= {Phytochemical Analysis}, volume= {28}, number= {3}, pages= {230-241}, keywords= {Paclitaxel resistance, β-tubulin, alkaloids, DataWarrior, LD50, scaffolds}, doi= {https://doi.org/10.1002/pca.2665}, url= {https://analyticalsciencejournals.onlinelibrary.wiley.com/doi/abs/10.1002/pca.2665}, eprint= {https://analyticalsciencejournals.onlinelibrary.wiley.com/doi/pdf/10.1002/pca.2665}, abstract= {Abstract Introduction β-Tubulin is an important target for the binding of anti-cancer drugs, in particular, paclitaxel (taxol), vinblastine and epothilone. However, mutations in β-tubulin structure give resistance to chemotherapeutic agents. Notably, mutations at R306C, F270 V, L217R, L228F, A185T and A248V positions in β-tubulin give high resistance for paclitaxel binding. Objective To discover novel inhibitors of β-tubulin from natural sources, particularly alkaloids, using a virtual screening approach. Methodology A virtual screening approach was employed to find potent lead molecules from the Naturally-occurring Plant-based Anti-cancer Compound-activity Target (NPACT) database. Alkaloids have great potential to be anti-cancer agents. Therefore, we have screened all alkaloids from a total of 1574 molecules from the NPACT database for our study. Initially, Molinspiration and DataWarrior programs were utilised to calculate pharmacokinetics and toxicity risks of the alkaloids, respectively. Subsequently, AutoDock algorithm was employed to understand the binding efficiency of alkaloids against β-tubulin. The binding affinity of the docked complex was confirmed by means of an intermolecular interaction study. Moreover, oral toxicity was predicted by using ProTox program. Further, metabolising capacity of drugs was studied by using SmartCYP software. Additionally, scaffold analysis was done with the help of scaffold trees and dendrograms, providing knowledge about the building blocks for parent-compound synthesis. Results Overall, the results of our computational analysis indicate that isostrychnine, obtained from Strychnosnux-vomica, satisfies pharmacokinetic and bioavailability properties, binds efficiently with β-tubulin. Thus, it could be a promising lead for the treatment of paclitaxel resistant cancer types. Conclusion This is the first observation of inhibitory activity of isostrychnine against β-tubulin and warrants further experimental investigation. Copyright © 2016 John Wiley \& Sons, Ltd.}, year= {2017}} . Phytochemical Analysis.

Investigation of Paclitaxel Resistant R306C Mutation in β-Tubulin—A Computational Approach @article{https://doi.org/10.1002/jcb.25087, author= {Verma, Kanika and Ramanathan, K.}, title= {Investigation of Paclitaxel Resistant R306C Mutation in β-Tubulin—A Computational Approach}, journal= {Journal of Cellular Biochemistry}, volume= {116}, number= {7}, pages= {1318-1324}, keywords= {PACLITAXEL, R306C MUTATION, MOLECULAR DOCKING, MOLECULAR DYNAMICS}, doi= {https://doi.org/10.1002/jcb.25087}, url= {https://onlinelibrary.wiley.com/doi/abs/10.1002/jcb.25087}, eprint= {https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcb.25087}, abstract= {ABSTRACT Paclitaxel is the most effective chemotherapeutic agent used for the treatment of a broad spectrum of solid tumors. However, observed paclitaxel resistance in clinical trials presents one of the major obstacles for cancer chemotherapy. Most importantly, resistance due to β-tubulin mutations (R306C) has been intensely debated in recent years. Despite all efforts, mechanism of resistance is still not well understood. In this study, computational techniques were employed to uncover the effect of R306C mutation in the β-tubulin structure and its function. The tools such as I-Mutant, CUPSAT and Fold-X were employed to address the consequence of R306C mutation in the structural stability of β-tubulin. Further, molecular docking and molecular dynamics study was employed to understand the functional impact of β-tubulin mutation. Our results suggest that the R306C mutation causes a significant reduction in the binding affinity between β-tubulin and paclitaxel. Further, docked complex analysis indicates that destruction of conservative hydrogen bond maintained by the residues Arg282 and Gly360 should be responsible for the large conformation changes of the binding pocket in R306C mutant. Finally, molecular dynamics simulations study confirms the stable binding of paclitaxel with native type β-tubulin structure rather than mutant (R306C) type. We certainly believe that this study will provide useful guidance for the development of novel inhibitors that are less susceptible to drug resistance. J. Cell. Biochem. 116: 1318–1324, 2015. © 2015 Wiley Periodicals, Inc.}, year= {2015}} . Journal of Cellular Biochemistry.