Navnath Gavande

Navnath Gavande

Wayne State University

H-index: 20

North America-United States

About Navnath Gavande

Navnath Gavande, With an exceptional h-index of 20 and a recent h-index of 16 (since 2020), a distinguished researcher at Wayne State University, specializes in the field of Pharmaceutical Drug Discovery: Medicinal/Organic Chemistry, Pharmacology/Chemical Biology, Pharmaceutical Sciences..

His recent articles reflect a diverse array of research interests and contributions to the field:

Abstract 1713 Shaping antiviral strategies with potent and selective non-covalent SARS-CoV-2 papain-like protease inhibitors

Abstract A027: Development of small molecule inhibitors of the Ku-DNA interaction: Impacts on NHEJ, DDR signaling, optimizing genome editing technologies, and therapeutic …

Abstract B020: Targeting the DNA damage response sensor Replication Protein A for first in class cancer therapy

Novel Ku-DNA binding inhibitors impact on the cellular and in vivo DNA damage response to radio- and radiomimetic-therapy

Development of substituted oxindole derivatives as a Ku-targeted DNA-PK inhibitors for cancer therapy

Compositions and methods relating to inhibitors of pro-inflammatory factors for treatment of cancer

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Replication protein a (rpa)-dna interaction inhibitors

Navnath Gavande Information

University

Wayne State University

Position

Assistant Professor College of Pharmacy Detroit Michigan USA

Citations(all)

1502

Citations(since 2020)

876

Cited By

951

hIndex(all)

20

hIndex(since 2020)

16

i10Index(all)

32

i10Index(since 2020)

22

Email

University Profile Page

Wayne State University

Navnath Gavande Skills & Research Interests

Pharmaceutical Drug Discovery: Medicinal/Organic Chemistry

Pharmacology/Chemical Biology

Pharmaceutical Sciences.

Top articles of Navnath Gavande

Abstract 1713 Shaping antiviral strategies with potent and selective non-covalent SARS-CoV-2 papain-like protease inhibitors

Authors

Abdullah Al-Homoudi,Hariprased Aruri,Dineshsinha Chauhan,Olivia Haskin,Jacob Tartamella,Joseph Engel,Navnath Gavande,Ladislau Kovari

Journal

Journal of Biological Chemistry

Published Date

2024/3/1

SARS-CoV-2 continues to elude containment efforts and remains a significant global health challenge. There is a critical need for drugs that employ multiple mechanisms of action, ensuring a more robust and versatile approach to effectively manage both current and emerging coronavirus infections. The papain-like protease (PLpro) domain of Nsp3 is essential for viral replication in human coronaviruses (HCoV). PLpro also contributes to the COVID-19-associated ‘cytokine storm’by cleaving ubiquitin and interferon-stimulated gene 15 protein (ISG15) from host proteins and disrupting host immune responses. Consequently, PLpro is a promising target for small-molecule therapeutics. In this study, we have refined non-covalent inhibitors of SARS-CoV-1 PLpro and SARS-CoV-2 PLpro from primary literature, resulting in a lead inhibitor with improved cytotoxicity values and specificity towards SARS-CoV-1 and SARS …

Abstract A027: Development of small molecule inhibitors of the Ku-DNA interaction: Impacts on NHEJ, DDR signaling, optimizing genome editing technologies, and therapeutic …

Authors

John J Turchi,Pamela L Mendoza-Munoz,Pamela S VanderVere-Carozza,Navnath S Gavande,Joseph R Dynlacht,Joy E Garrett,Dineshsinha Chauhan,Katherine S Pawelczak

Journal

Cancer Research

Published Date

2024/1/9

DNA-PK, the DNA-dependent protein kinase is a validated target for cancer therapeutics that drives the DNA damage response (DDR) and plays a critical role in the non-homologous end joining (NHEJ) DNA repair pathway. NHEJ is responsible for the repair of DNA double strand breaks (DSB), particularly those induced by ionizing radiation (IR). The generation of DNA DSBs drives clinical efficacy of radiation therapy and numerous DNA damaging chemotherapeutic drugs used to treat cancer. Modulating the DSB repair pathways is an effective mechanism to increase clinical efficacy of IR and certain chemotherapeutic regimens. We have taken the novel approach to inhibit target the DDR and NHEJ by developing small molecule inhibitors of the DSB sensor Ku, and its interaction with DNA. The Ku heterodimer serves as initiator of the NHEJ pathway following DSB induction and is the key DNA-binding component …

Abstract B020: Targeting the DNA damage response sensor Replication Protein A for first in class cancer therapy

Authors

Katherine Pawelczak,Pamela VanderVere-Carozza,Matthew Jordon,Navnath Gavande,John Turchi

Journal

Cancer Research

Published Date

2024/1/9

The DNA Damage Response (DDR) is a DNA repair and cell signaling pathway crucial in maintaining genomic stability. The most successful DDR targeted therapies inhibit the DNA damage sensor, PARP, a protein that recognizes single strand DNA (ssDNA) breaks as well as other DNA secondary structures induced by single strand gaps that can initiate chromosome instability and cell death. Building on the initial clinical success of PARP inhibitors, development of DDR targeted therapeutics has become increasingly popular with the majority of new agents targeting protein kinases downstream of the DNA damage sensors. The clinical outcomes with these therapeutics have not met expectations and thus a new approach to targeting the DDR pathway is needed. NERx Biosciences has developed a novel strategy of targeting the DDR by intervening upstream of the DDR kinases and targeting specific DDR sensors …

Novel Ku-DNA binding inhibitors impact on the cellular and in vivo DNA damage response to radio- and radiomimetic-therapy

Authors

Pamela L Mendoza-Munoz,Dineshsinha Chauhan,Navnath S Gavande,Joseph R Dynlacht,Joy E Garrett,John J Turchi

Journal

Cancer Research

Published Date

2024/3/22

DNA-PK, the DNA-dependent protein kinase, is a validated target for cancer therapeutics that plays a central role in the non-homologous end joining (NHEJ) DNA repair pathway and the DNA damage response (DDR). NHEJ is a key mechanism of DNA double-strand breaks (DSB) repair, especially those induced by ionizing radiation (IR). Ku 70/80 heterodimer is required as initiator in this process, acting as an essential DNA-binding component of DNA-PK that senses DNA damage. Blocking the DNA-PK kinase activity in combination with DSB inducing agents has been widely used as a therapeutic strategy to drive clinical efficacy of radiation therapy for cancer treatment. We have reported a unique approach of DNA-PK inhibition by developing Ku-DNA binding inhibitors (Ku-DBi’s), small molecule inhibitors that target the interaction between Ku70/80 and DNA. Ku-DBi’s demonstrated a direct interaction with Ku70 …

Development of substituted oxindole derivatives as a Ku-targeted DNA-PK inhibitors for cancer therapy

Authors

Dineshsinha Chauhan,Pamela L Mendoza-Munoz,Narva Deshwar Kushwaha,Hariprasad Aruri,John J Turchi,Navnath S Gavande

Journal

Cancer Research

Published Date

2024/3/22

DNA double strand breaks (DSBs) are the most cytotoxic type of DNA damage. DSB repair pathway deficiency, often observed in cancer cells, results in translocations and genetic mutations that contribute to genomic instability. The generation of DNA DSBs is the primary mechanism of numerous chemo- and radio-therapeutic strategies used to treat various cancers. Modulating DSB repair pathways can have a profound impact on the clinical efficacy of DNA damaging therapies. DNA-dependent protein kinase (DNA-PK), which is composed of a DNA-PK catalytic subunit (DNA-PKcs) and Ku80-Ku70 heterodimer, acts as the molecular sensor for DSB and plays a prime role in DSB repair through non-homologous end joining (NHEJ). DNA-PK inhibitors become an attractive therapeutic target for cancer in combination with DSB-inducing radiotherapy and chemotherapy. There are at least 6-7 DNA-PK inhibitors in the …

Compositions and methods relating to inhibitors of pro-inflammatory factors for treatment of cancer

Published Date

2024/3/19

XKTZWUACRZHVAN-VADRZIEHSA-N interleukin-8 Chemical compound C ([C@ H](NC (= O)[C@ H](CC (O)= O) NC (= O)[C@ H](CC= 1C2= CC= CC= C2NC= 1) NC (= O)[C@@ H](NC (C)= O) CCSC) C (= O) N [C@@ H](CC (O)= O) C (= O) N [C@@ H](CC (O)= O) C (= O) N [C@@ H](CC (C) C) C (= O) N [C@@ H](CC (N)= O) C (= O) N [C@@ H](CC= 1C= CC= CC= 1) C (= O) N [C@@ H]([C@@ H](C) O) C (= O) NCC (= O) N [C@@ H](CCSC) C (= O) N1 [C@ H](CCC1) C (= O) N1 [C@ H](CCC1) C (= O) N [C@@ H](C) C (= O) N [C@ H](CC (O)= O) C (= O) N [C@ H](CCC (O)= O) C (= O) N [C@ H](CC (O)= O) C (= O) N [C@ H](CC= 1C= CC (O)= CC= 1) C (= O) N [C@ H](CO) C (= O) N1 [C@ H](CCC1) C (N)= O) C1= CC= CC= C1 XKTZWUACRZHVAN-VADRZIEHSA-N 0.000 description 25

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Authors

José Luis Losada,Asier Gonzalez-Artetxe,Yousri Elghoul,Júlio A Costa,JA Costa,V Rago,P Brito,P Figueiredo,A Sousa,E Abade,J Brito

Journal

Community Series-Extremophiles: Microbial Genomics and Taxogenomics, Volume II

Published Date

2023/11/22

Objective: The present systematic review aimed to provide an overview of training load (TL), along with their responses, monitoring during training sessions in highly trained and elite adult women soccer players.Data source: Electronic databases searches (PubMed, Scopus, Web of Science and Ebsco) for relevant studies published in peer-reviewed journals were conducted, and eligibility criteria were based on the PICOS model in accordance with PRISMA guidelines.Study selection: Studies were considered as follows:(a) highly trained and elite adult (> 18 years) women's soccer players;(b) continuous (minimum1-week duration) TL monitoring in the context of the team routine;(c) TL collected from entire training session. Methodological qualitative assessments and risk of bias criteria were used for judging the studies.Data extraction: A total of 1,163 studies were identified, and 16 were included. The selected studies were fully screened to extract the population characteristics; the number of players; a type of study design; region where the study was performed; the main findings.Data synthesis: Accumulated external TL (ETL) during the pre-season was positively correlated to enhanced adaptations in intermittent exercise capacity. Daily ETL was negatively correlated to next-day self-reported fatigue and muscle soreness. Daily internal TL (ITL) was negatively correlated to postsession sleep duration and sleep efficiency. One study showed that higher accumulated player load and total distance were associated with injury.

Replication protein a (rpa)-dna interaction inhibitors

Published Date

2023/2/23

This invention relates to RPA compounds or pharmaceutically acceptable salts thereof, and for the use of the compounds to treat cancer.

Leveraging hypoxia in triple-negative breast cancer as a promising treatment strategy

Authors

Ketki Bhise,Navnath S Gavande,Arun K Iyer

Published Date

2023/9/1

Current treatment strategies for triple-negative breast cancer (TNBC) are based upon conventional chemotherapy, immunotherapy, or a combination of both. The treatment regimen for chemotherapy is often a combination of two or more drugs, either dose dense or low dose for synergy. Anthracyclines, alkylating agents, antimicrotubule agents, and antimetabolites for early-stage TNBC; and antimetabolites, non-taxane microtubule inhibitors, and cross-linker platinums for late-stage TNBC are usually administered in the clinical setting. Newer options for patients with advanced TNBC, such as poly (ADP-ribose) polymerase (PARP) inhibitors and immune checkpoint inhibitors, have recently emerged for cases where surgery is not a viable option and the disease has metastasized. This review outlines the current trends in hypoxia-inspired treatment strategies for TNBC with a focus on clinical trials.Teaser:This review …

Targeting the epidermal growth factor receptor with molecular degraders: State-of-the-art and future opportunities

Authors

Pritam Maity,Joydeep Chatterjee,Kiran T Patil,Sahil Arora,Madhurendra K Katiyar,Manvendra Kumar,Amirreza Samarbakhsh,Gaurav Joshi,Priyadeep Bhutani,Manoj Chugh,Navnath S Gavande,Raj Kumar

Published Date

2023/2/22

Epidermal growth factor receptor (EGFR) is an oncogenic drug target and plays a critical role in several cellular functions including cancer cell growth, survival, proliferation, differentiation, and motility. Several small-molecule tyrosine kinase inhibitors (TKIs) and monoclonal antibodies (mAbs) have been approved for targeting intracellular and extracellular domains of EGFR, respectively. However, cancer heterogeneity, mutations in the catalytic domain of EGFR, and persistent drug resistance limited their use. Different novel modalities are gaining a position in the limelight of anti-EGFR therapeutics to overcome such limitations. The current perspective reflects upon newer modalities, importantly the molecular degraders such as PROTACs, LYTACs, AUTECs, and ATTECs, etc., beginning with a snapshot of traditional and existing anti-EGFR therapies including small molecule inhibitors, mAbs, and antibody drug …

Senescence-associated secretory proteins induced in lung adenocarcinoma by extended treatment with dexamethasone enhance migration and activation of lymphocytes

Authors

Prahlad Parajuli,Rayna Rosati,Hirva Mamdani,Robert E Wright III,Zahin Hussain,Aroma Naeem,Sijana Dzinic,Lisa Polin,Navnath S Gavande,Manohar Ratnam

Journal

Cancer Immunology, Immunotherapy

Published Date

2023/5

There is a need to improve response rates of immunotherapies in lung adenocarcinoma (AC). Extended (7–14 days) treatment of high glucocorticoid receptor (GR) expressing lung AC cells with dexamethasone (Dex) induces an irreversible senescence phenotype through chronic induction of p27. As the senescence-associated secretory phenotype (SASP) may have either tumor supporting or antitumor immunomodulatory effects, it was interest to examine the effects of Dex-induced senescence of lung AC cells on immune cells. Dex-induced senescence resulted in sustained production of CCL2, CCL4, CXCL1 and CXCL2, both in vitro and in vivo. After Dex withdrawal, secretion of these chemokines by the senescent cells attracted peripheral blood monocytes, T-cells, and NK cells. Following treatment with Dex-induced SASP protein(s), the peripheral blood lymphocytes exhibited higher cell count and tumor …

Identification of novel inhibitors targeting KRAS-SOS1 interactions by structure-based drug design

Authors

Neel A Patel,Timothy Hasse,Evan Malin,Jeremy M Kelm,Navnath Gavande,Yu-ming Huang

Journal

Biophysical Journal

Published Date

2023/2/10

The Kristen Rat Sarcoma (KRAS) protein, encoded by the KRAS gene, is a signal transducer that plays a crucial role in regulating cell proliferation. KRAS mutations have been known to cause lung, colorectal, and pancreatic cancers. Previously, KRAS was considered an" undruggable" target. However, with a better understanding of the protein's biology paired with advanced new technologies, the FDA approved the first KRAS inhibitor (sotorasib) for lung cancer patients with the KRASG12C mutation in 2021, expressing the recent interest of targeted drugs for KRAS. Oncogenic KRAS requires activation by the guanine nucleotide exchange factor (GEF) Son of Sevenless 1 (SOS1). The goal of this study is to develop novel pan-KRAS inhibitors by targeting the KRAS-SOS1 interactions through computational modeling. To start, we applied Gaussian accelerated molecular dynamics (GaMD) simulation, an advanced …

Abstract B052: Small molecule RPA inhibitors abrogate the ATR kinase signaling pathway

Authors

Matthew R Jordan,Diana Ainembabazi,Pamela S VanderVere-Carozza,Navnath S Gavande,Katherine S Pawelczak,John J Turchi

Journal

Molecular Cancer Therapeutics

Published Date

2023/12/1

Replication Protein A (RPA) is the major single-stranded DNA (ssDNA) binding protein in the cell and plays a role in replication, recombination, and the DNA damage response (DDR) and repair. RPA functions to protect ssDNA from degradation and also serves as an interaction hub to recruit replication and DDR machinery. Under normal cellular conditions, RPA protein abundance is in excess to that of the ssDNA generated during S phase replication so as to protect from replication fork collapse and replication catastrophe in the event of elevated levels of replication stress. RPA inhibition is thus a promising cancer therapeutic strategy that targets oncogenic cells with increased replication stress due to rapid cell proliferation, genotoxic stressors, DDR inhibition, etc, and therefore an increased ssDNA burden. We have previously developed the RPA inhibitor (RPAi) NERx329 that disrupts RPA-ssDNA binding and …

PROTAC’ing oncoproteins: targeted protein degradation for cancer therapy

Authors

Jeremy M Kelm,Deepti S Pandey,Evan Malin,Hussein Kansou,Sahil Arora,Raj Kumar,Navnath S Gavande

Published Date

2023/3/30

Molecularly targeted cancer therapies substantially improve patient outcomes, although the durability of their effectiveness can be limited. Resistance to these therapies is often related to adaptive changes in the target oncoprotein which reduce binding affinity. The arsenal of targeted cancer therapies, moreover, lacks coverage of several notorious oncoproteins with challenging features for inhibitor development. Degraders are a relatively new therapeutic modality which deplete the target protein by hijacking the cellular protein destruction machinery. Degraders offer several advantages for cancer therapy including resiliency to acquired mutations in the target protein, enhanced selectivity, lower dosing requirements, and the potential to abrogate oncogenic transcription factors and scaffolding proteins. Herein, we review the development of proteolysis targeting chimeras (PROTACs) for selected cancer therapy …

Benzene fused pyrimidine-based derivatives and their biological properties

Authors

Jeremy M Kelm,Hariprasad Aruri,Prasanth R Nyalapatla,Navnath S Gavande

Published Date

2023/1/1

Benzene fused pyrimidine (quinazoline) is widely utilized as a bioactive scaffold during the development of drugs for a multitude of disease states. The quinazoline scaffold has enjoyed routine use in the design of kinase inhibitors because of its adaptability to selectively engage a desired ATP-binding pocket. The medicinal chemistry applications of the quinazoline scaffold have expanded to include drugging cellular surface proteins including Toll like receptor 7/8, IKur, and P-glycoprotein, as well as intracellular nonkinase targets such as tubulin. The spatial orientation of the quinazoline core while bound to ATP-binding pockets has permitted the successful bifunctionalization through substitution of positions 6 and 7. The two nitrogens present in the quinazoline scaffold prove useful for improving drug solubility, drug-like properties, and commonly engage the target protein via hydrogen bonding interactions. This …

Ku–DNA binding inhibitors modulate the DNA damage response in response to DNA double-strand breaks

Authors

Pamela L Mendoza-Munoz,Navnath S Gavande,Pamela S VanderVere-Carozza,Katherine S Pawelczak,Joseph R Dynlacht,Joy E Garrett,John J Turchi

Journal

NAR cancer

Published Date

2023/3/1

The DNA-dependent protein kinase (DNA-PK) plays a critical role in the DNA damage response (DDR) and non-homologous end joining (NHEJ) double-strand break (DSB) repair pathways. Consequently, DNA-PK is a validated therapeutic target for cancer treatment in certain DNA repair-deficient cancers and in combination with ionizing radiation (IR). We have previously reported the discovery and development of a novel class of DNA-PK inhibitors with a unique mechanism of action, blocking the Ku 70/80 heterodimer interaction with DNA. These Ku–DNA binding inhibitors (Ku-DBi's) display nanomolar activity in vitro, inhibit cellular DNA-PK, NHEJ-catalyzed DSB repair and sensitize non-small cell lung cancer (NSCLC) cells to DSB-inducing agents. In this study, we demonstrate that chemical inhibition of the Ku–DNA interaction potentiates the cellular effects of bleomycin and IR via p53 phosphorylation …

Abstract B068: Modulation of the DNA damage response by novel Ku-DNA binding inhibitors enhances cellular effects of DNA-double strand break inducing agents

Authors

Pamela L Mendoza-Munoz,Dineshsinha Chauhan,Navnath S Gavande,John J Turchi

Journal

Molecular Cancer Therapeutics

Published Date

2023/12/1

The DNA-dependent protein kinase (DNA-PK) plays a critical role in the non-homologous end joining (NHEJ) double-strand break (DSB) repair pathway and the DNA damage response (DDR). Consequently, blocking DNA-PK kinase activity is being pursued as a therapeutic strategy for the treatment of cancer in combination with DNA-double strand break inducing agents. We have previously reported the development of Ku-DNA binding inhibitors (Ku-DBi’s) that act via a novel mechanism of action to inhibit DNA-PK catalytic kinase activity by targeting the Ku 70/80 heterodimer interaction with DNA. Ku-DBi’s display nanomolar activity in vitro, possess cellular DNA-PK and NHEJ inhibitory activity, and sensitize non-small cell lung cancer (NSCLC) cells to DSB generating therapies bleomycin, etoposide and ionizing radiation. In this study, we have expanded our structure activity relationship analyses to focus on …

Nanomedicine approaches to reduce cytokine storms in severe infections

Authors

Mohd Ahmar Rauf,Maryam Nisar,Hosam Abdelhady,Navnath Gavande,Arun K Iyer

Published Date

2022/11/1

HighlightsCytokine storm causes dysregulated production of a wide range of pro-inflammatory cytokines.Cytokine storm is associated with many infectious diseases including COVID-19.Nanomedicine based therapies have potential to treat cytokine storm in infections.During a cytokine storm, dysregulated proinflammatory cytokines are produced in excess. Cytokine storms occur in multiple infectious diseases, including Coronavirus 2019 (COVID-19). Thus, eliminating cytokine storms to enhance patient outcomes is crucial. Given the numerous cytokines involved, individual therapies might have little effect. Traditional cytokines might be less effective than medicines that target malfunctioning macrophages. Nanomedicine-based therapeutics reduce cytokine production in animal models of proinflammatory illnesses. The unique physicochemical features and controlled nano–bio interactions of nanotechnology show …

Recent advances in the development of non-PIKKs targeting small molecule inhibitors of DNA double-strand break repair

Authors

Jeremy M Kelm,Amirreza Samarbakhsh,Athira Pillai,Pamela S VanderVere-Carozza,Hariprasad Aruri,Deepti S Pandey,Katherine S Pawelczak,John J Turchi,Navnath S Gavande

Published Date

2022/4/6

The vast majority of cancer patients receive DNA-damaging drugs or ionizing radiation (IR), yet the efficacy of these therapies is tempered by DNA repair and DNA damage response (DDR) pathways. Aberrations of DNA repair and the DDR are observed in every cancer subtype which promote de novo carcinogenesis, genomic instability, and ensuing resistance to current cancer therapy. Additionally, stalled or collapsed DNA replication forks present a catastrophic challenge to the double-strand DNA break (DSB) repair system. Of the various inducible DNA lesions, DSBs are the most lethal and thus desirable in the setting of cancer treatment. In mammalian cells, DSBs are typically repaired by the non-homologous end joining pathway (NHEJ) or the high-fidelity homology directed repair (HDR) pathway. Targeting DSB repair pathways using small molecular inhibitors offers a promising mechanism to synergize DNA-damaging drugs and IR while selective inhibition of the NHEJ pathway can induce synthetic lethality in HDR-deficient cancer subtypes. Selective inhibitors of the NHEJ pathway and alternative DSB-repair pathways may also see future use in precision genome editing to direct repair of the DSBs created by the HDR pathway. In this review, we highlight the recent advances in the development of inhibitors of the non-phosphatidylinositol 3-kinase-related kinases (non-PIKKs) members of the NHEJ, HDR and minor backup SSA and alt-NHEJ DSB-repair pathways. The targeted inhibitors described within the non-PIKKs DSB repair mediators including Ku70/80, Artemis, DNA Ligase IV, XRCC4, MRN complex, RPA, RAD51, RAD52, ERCC1 …

Ku-DNA binding inhibitors modulate the DNA damage response in response to DNA double-strand breaks

Authors

P Mendoza-Munoz,NS Gavande,PS VanderVere-Carozza,KS Pawelczak,JR Dynlacht,JE Garrett,JJ Turchi

Journal

European Journal of Cancer

Published Date

2022/10/1

Background: The DNA-dependent protein kinase (DNA-PK) plays a critical role in the non-homologous end joining (NHEJ) double-strand break (DSB) repair pathway and the DNA damage response (DDR). Consequently, blocking DNA-PK kinase activity is being pursued as a therapeutic strategy for the treatment of cancer in combination with ionizing radiation (IR). Towards developing a new class of DNA-PK inhibitors, our laboratory previously reported the development of Ku-DNA binding inhibitors (Ku-DBis) that act via inhibition of DNA-PK catalytic kinase activity by blocking the Ku-DNA interaction. Ku-DBis display nanomolar activity in vitro, possess cellular DNA-PK and NHEJ inhibitory activity, and sensitize non-small cell lung cancer (NSCLC) cells to DSB generating chemotherapeutics bleomycin and etoposide.Material and Methods: Using multiple NSCLC cell lines possessing mutations in specific DDR …

See List of Professors in Navnath Gavande University(Wayne State University)

Navnath Gavande FAQs

What is Navnath Gavande's h-index at Wayne State University?

The h-index of Navnath Gavande has been 16 since 2020 and 20 in total.

What are Navnath Gavande's top articles?

The articles with the titles of

Abstract 1713 Shaping antiviral strategies with potent and selective non-covalent SARS-CoV-2 papain-like protease inhibitors

Abstract A027: Development of small molecule inhibitors of the Ku-DNA interaction: Impacts on NHEJ, DDR signaling, optimizing genome editing technologies, and therapeutic …

Abstract B020: Targeting the DNA damage response sensor Replication Protein A for first in class cancer therapy

Novel Ku-DNA binding inhibitors impact on the cellular and in vivo DNA damage response to radio- and radiomimetic-therapy

Development of substituted oxindole derivatives as a Ku-targeted DNA-PK inhibitors for cancer therapy

Compositions and methods relating to inhibitors of pro-inflammatory factors for treatment of cancer

OPEN ACCESS EDITED BY

Replication protein a (rpa)-dna interaction inhibitors

...

are the top articles of Navnath Gavande at Wayne State University.

What are Navnath Gavande's research interests?

The research interests of Navnath Gavande are: Pharmaceutical Drug Discovery: Medicinal/Organic Chemistry, Pharmacology/Chemical Biology, Pharmaceutical Sciences.

What is Navnath Gavande's total number of citations?

Navnath Gavande has 1,502 citations in total.

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