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Article ; Online: Matrix-Metalloproteinase Inhibitory Study of Novel Tetrahydroisoquinoline-4-carboxylates: Design, Synthesis, and Molecular Docking Studies.

Devappa Satyanarayan, Nayak / Kammathalli Siddappa, Manjunatha / Rahman, Abdul / Belur Ningegowda, Nippu / Sherapura, Ankith / Siddesh, B M / Prabhakar, B T

Chemistry & biodiversity

2023 Volume 20, Issue 5, Page(s) e202201152

Abstract: The design, molecular docking, synthesis and structure-activity relationship (SAR) of a series of novel methyl 1-oxo-2-(propan-2-yl)-3-(pyridin-3-yl)-1,2,3,4-tetrahydroisoquinoline-4-carboxylates, were investigated for antiproliferative and cytotoxic ... ...

Abstract	The design, molecular docking, synthesis and structure-activity relationship (SAR) of a series of novel methyl 1-oxo-2-(propan-2-yl)-3-(pyridin-3-yl)-1,2,3,4-tetrahydroisoquinoline-4-carboxylates, were investigated for antiproliferative and cytotoxic studies by screening against cancer cell lines of different origin by MTT, LDH and Trypan Blue Assay. Irrespective of cell lines, among the synthesized nonpeptido-mimetic analogs 5a-e, 5c has executed potent bio-potency with IC
MeSH term(s)	Animals ; Mice ; Molecular Structure ; Molecular Docking Simulation ; Cell Line, Tumor ; Cell Proliferation ; Drug Screening Assays, Antitumor ; Structure-Activity Relationship ; Antineoplastic Agents/pharmacology ; Tetrahydroisoquinolines/pharmacology ; Metalloproteases/pharmacology ; Drug Design ; Protein Kinase Inhibitors/pharmacology
Chemical Substances	Antineoplastic Agents ; Tetrahydroisoquinolines ; Metalloproteases (EC 3.4.-) ; Protein Kinase Inhibitors
Language	English
Publishing date	2023-04-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2139001-0
ISSN	1612-1880 ; 1612-1872
ISSN (online)	1612-1880
ISSN	1612-1872
DOI	10.1002/cbdv.202201152
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Steroidal alkaloid solanidine impedes hypoxia-driven ATM phosphorylation to switch on anti-angiogenesis in lung adenocarcinoma.

Sherapura, Ankith / Siddesh, B M / Malojirao, Vikas H / Thirusangu, Prabhu / Avin, B R Vijay / Kumari, N Suchetha / Ramachandra, Y L / Prabhakar, B T

Phytomedicine : international journal of phytotherapy and phytopharmacology

2023 Volume 119, Page(s) 154981

Abstract: Purpose: The declined oxygen tension in the cancer cell leads to the hypoxic adaptive response and favors establishment of tumor micro environment [TEM]. The complex TME consists of interwoven hypoxic HIF-1α and DNA damage repair ATM signaling. The ATM/ ... ...

Abstract	Purpose: The declined oxygen tension in the cancer cell leads to the hypoxic adaptive response and favors establishment of tumor micro environment [TEM]. The complex TME consists of interwoven hypoxic HIF-1α and DNA damage repair ATM signaling. The ATM/HIF-1α phosphorylation switch on angiogenesis and abort apoptosis. Targeting this signaling nexus would be a novel therapeutic strategy for the treatment of cancer. Background: Steroidal alkaloid solanidine is known for varied pharmacological role but with less molecular evidences. Our earlier findings on solanidine proven its anti-neoplastic activity by inducing apoptosis in lung cancer. In continued research, efforts have been made to establish the underlying molecular signaling in induction of DNA damage in prevailing hypoxic TME. Methods: The solanidine induced DNA damage was assessed trough alkali COMET assay; signaling nexus and gene expression profile analysis through IB, qRT-PCR, Gelatin Zymography, IHC, IF and ELISA. Pathophysiological modulations assessed through tube formation, migration, invasion assays. Anti-angiogenic studies through CAM, rat aorta, matrigel assays and corneal neovascularization assay. Anti-tumor activity through in-vivo DLA ascites tumor model and LLC model. Results: The results postulates, inhibition of hypoxia driven DDR proteins pATM
MeSH term(s)	Rats ; Animals ; Phosphorylation ; Antineoplastic Agents/therapeutic use ; Hypoxia/drug therapy ; Alkaloids/pharmacology ; Adenocarcinoma of Lung/drug therapy ; Lung Neoplasms/drug therapy ; Hypoxia-Inducible Factor 1, alpha Subunit ; Neovascularization, Pathologic/drug therapy ; Cell Line, Tumor ; Tumor Microenvironment
Chemical Substances	solanidine (W7801OHM8B) ; Antineoplastic Agents ; Alkaloids ; Hypoxia-Inducible Factor 1, alpha Subunit
Language	English
Publishing date	2023-07-18
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1205240-1
ISSN	1618-095X ; 0944-7113
ISSN (online)	1618-095X
ISSN	0944-7113
DOI	10.1016/j.phymed.2023.154981
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Article ; Online: Steroidal alkaloid solanidine impedes hypoxia-driven ATM phosphorylation to switch on anti-angiogenesis in lung adenocarcinoma

Sherapura, Ankith / Siddesh, B.M. / Malojirao, Vikas H. / Thirusangu, Prabhu / Avin, B.R. Vijay / Kumari, N Suchetha / Ramachandra, Y.L. / Prabhakar, B.T.

Phytomedicine. 2023 July 18, p.154981-

2023 , Page(s) 154981–

Abstract: The declined oxygen tension in the cancer cell leads to the hypoxic adaptive response and favors establishment of tumor micro environment [TEM]. The complex TME consists of interwoven hypoxic HIF-1α and DNA damage repair ATM signaling. The ATM/HIF-1α ... ...

Abstract	The declined oxygen tension in the cancer cell leads to the hypoxic adaptive response and favors establishment of tumor micro environment [TEM]. The complex TME consists of interwoven hypoxic HIF-1α and DNA damage repair ATM signaling. The ATM/HIF-1α phosphorylation switch on angiogenesis and abort apoptosis. Targeting this signaling nexus would be a novel therapeutic strategy for the treatment of cancer. Steroidal alkaloid solanidine is known for varied pharmacological role but with less molecular evidences. Our earlier findings on solanidine proven its anti-neoplastic activity by inducing apoptosis in lung cancer. In continued research, efforts have been made to establish the underlying molecular signaling in induction of DNA damage in prevailing hypoxic TME. The solanidine induced DNA damage was assessed trough alkali COMET assay; signaling nexus and gene expression profile analysis through by IB, qRT-PCR, Gelatin Zymography, IHC, IF and ELISA. Pathophysiological modulations assessed through tube formation, migration, invasion assays. Anti-angiogenic studies through CAM, rat aorta, matrigel assays and corneal neo-vascularization assay. Anti-tumor activity through in-vivo DLA ascites tumor model and LLC model. The results postulates, inhibition of hypoxia driven DDR proteins pATMˢᵉʳ¹⁹⁸¹/pHIF-1αˢᵉʳ⁶⁹⁶ by solanidine induces anti-angiogenesis. Systematic study of both non-tumorigenic and tumorigenic models in in-vitro as well as in-vivo experimental system revealed the angio-regression mediated anticancer effect in lung cancer. These effects are due to the impeded expression of angiogenic mediators such as VEGF, MMP2&9 and inflammatory cytokines IL6 and TNFα to induce pathophysiological changes The study establishes new role of solanidine by targeting ATM/HIF-1α signaling to induce anti-angiogenesis for the first time. The study highlights the potentiality of plant based phytomedicine solanidine which can targets the multiple hallmarks of cancer by targeting interwoven signaling crosstalk. Such an approach through solanidine necessary to counteract heterogeneous complexity of cancer which could be nearly translated into drug.
Keywords	DNA damage ; DNA repair ; adenocarcinoma ; angiogenesis ; antineoplastic activity ; aorta ; apoptosis ; ascites ; comet assay ; cornea ; drugs ; gelatin ; gene expression ; hypoxia ; interleukin-6 ; lung neoplasms ; lungs ; models ; neoplasm cells ; oxygen ; phosphorylation ; rats ; solanidine ; therapeutics ; TME ; lung cancer ; DDR ; ATM/HIF ; anti-angiogenesis ; ATM ; BER ; Chk2 ; DNA DSB ; DAPI 4′ ; ELISA ; ECM ; HIF-1α ; HRE ; HR ; IL6 ; LLC ; MMP 2&9 ; MVD ; TNFα ; VEGF ; XRCC1
Language	English
Dates of publication	2023-0718
Publishing place	Elsevier GmbH
Document type	Article ; Online
Note	Pre-press version
ZDB-ID	1205240-1
ISSN	1618-095X ; 0944-7113
ISSN (online)	1618-095X
ISSN	0944-7113
DOI	10.1016/j.phymed.2023.154981
Database	NAL-Catalogue (AGRICOLA)

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Article: A systems biology investigation of curcumin potency against TGF-β-induced EMT signaling in lung cancer.

Kandagalla, Shivananda / Sharath, B S / Sherapura, Ankith / Grishina, Maria / Potemkin, Vladimir / Lee, Julian / Ramaswamy, Gopalakrishna / Prabhakar, B T / Hanumanthappa, Manjunatha

3 Biotech

2022 Volume 12, Issue 11, Page(s) 306

Abstract: Curcumin (diferuloylmethane) is bioactive phenolic compound which exerts diverse antimetastatic effect. Several studies have reported the antimetastatic effect of curcumin by its ability to modulate the epithelial-to-mesenchymal transition (EMT) process ... ...

Abstract	Curcumin (diferuloylmethane) is bioactive phenolic compound which exerts diverse antimetastatic effect. Several studies have reported the antimetastatic effect of curcumin by its ability to modulate the epithelial-to-mesenchymal transition (EMT) process in different cancers, but underlying molecular mechanism is poorly understood. EMT is a highly conserved biological process in which epithelial cells acquire mesenchymal-like characteristics by losing their cell-cell junctions and polarity. As a consequence, deviation in cellular mechanism leads to cancer metastasis and thereby death. In this perspective, we explored the antimetastatic potential and mechanism of curcumin on the EMT process by establishing in vitro EMT model in lungs cancer (A549) cells induced by TGF-β1. Our results showed that curcumin mitigates EMT by regulating the expression of crucial mesenchymal markers such as MMP2, vimentin and N-cadherin. Besides, the transcriptional analysis revealed that the curcumin treatment differentially regulated the expression of 75 genes in NanoString nCounter platform. Further protein-protein interaction network and clusters analysis of differentially expressed genes revealed their involvement in essential biological processes that plays a key role during EMT transition. Altogether, the study provides a comprehensive overview of the antimetastatic potential of curcumin in TGF-β1-induced EMT in lung cancer cells. Supplementary information: The online version contains supplementary material available at 10.1007/s13205-022-03360-7.
Language	English
Publishing date	2022-10-01
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2600522-0
ISSN	2190-5738 ; 2190-572X
ISSN (online)	2190-5738
ISSN	2190-572X
DOI	10.1007/s13205-022-03360-7
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Article ; Online: Targeting HIF-1α by newly synthesized Indolephenoxyacetamide (IPA) analogs to induce anti-angiogenesis-mediated solid tumor suppression.

Al-Ostoot, Fares Hezam / Sherapura, Ankith / V, Vigneshwaran / Basappa, Giridhara / H K, Vivek / B T, Prabhakar / Khanum, Shaukath Ara

Pharmacological reports : PR

2021 Volume 73, Issue 5, Page(s) 1328–1343

Abstract: Background: Hypoxic microenvironment is a common feature of solid tumors, which leads to the promotion of cancer. The transcription factor, HIF-1α, expressed under hypoxic conditions stimulates tumor angiogenesis, favoring HIF-1α as a promising ... ...

Abstract	Background: Hypoxic microenvironment is a common feature of solid tumors, which leads to the promotion of cancer. The transcription factor, HIF-1α, expressed under hypoxic conditions stimulates tumor angiogenesis, favoring HIF-1α as a promising anticancer agent. On the other hand, synthetic Indolephenoxyacetamide derivatives are known for their pharmacological potentiality. With this background here, we have synthesized, characterized, and validated the new IPA (8a-n) analogs for anti-tumor activity. Methods: The new series of IPA (8a-n) were synthesized through a multi-step reaction sequence and characterized based on the different spectroscopic analysis FT-IR, Results: Screening for anti-proliferative studies inferred, IPA (8k) is a lead molecule with an IC Conclusion: The IPA (8k) is a potent anti-proliferative molecule with anti-angiogenic activity and specifically targets HIF1α, thereby modulates its downstream regulatory genes both in vitro and in vivo. The study provides scope for new target-specific drug development against HIF-1α for the treatment of solid tumors.
MeSH term(s)	Acetamides/chemical synthesis ; Acetamides/pharmacology ; Animals ; Antineoplastic Agents/chemical synthesis ; Antineoplastic Agents/pharmacology ; Gene Expression Regulation, Neoplastic/drug effects ; Human Umbilical Vein Endothelial Cells ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Lymphoma/drug therapy ; Mice ; Mice, Inbred BALB C ; Neovascularization, Pathologic/drug therapy ; Rats ; Rats, Wistar ; Signal Transduction ; Structure-Activity Relationship ; Xenograft Model Antitumor Assays
Chemical Substances	Acetamides ; Antineoplastic Agents ; Hif1a protein, rat ; Hypoxia-Inducible Factor 1, alpha Subunit
Language	English
Publishing date	2021-04-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2186248-5
ISSN	2299-5684 ; 1734-1140
ISSN (online)	2299-5684
ISSN	1734-1140
DOI	10.1007/s43440-021-00266-8
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Article: Modulation of DNA damage response by targeting ATM kinase using newly synthesized di-phenoxy acetamide (DPA) analogs to induce anti-neoplasia.

Al-Ostoot, Fares Hezam / Sherapura, Ankith / Malojirao, Vikas H / Thirusangu, Prabhu / Al-Muhimeed, Tahani I / Khanum, Shaukath Ara / Prabhakar, B T

Pharmacological reports : PR

2021 Volume 73, Issue 5, Page(s) 1344–1360

Abstract: Background: Imbalance and instability in the structure of the DNA have become major characteristics of cancer. In response to DNA damage, DNA damage response (DDR) protein, ataxia telangiectasia mutated (ATM), plays a pivotal role in the modulation of ... ...

Abstract	Background: Imbalance and instability in the structure of the DNA have become major characteristics of cancer. In response to DNA damage, DNA damage response (DDR) protein, ataxia telangiectasia mutated (ATM), plays a pivotal role in the modulation of regulatory regions responsible for inhibition of apoptosis, thereby neoplastic progression. Methods: A new series of DPA (7a-t) were synthesized, characterized. Anti-proliferative studies to identify the lead compound were carried out by LDH and MTT assay. Apoptosis/DNA damage was measured through FACS, Annexin-v staining, TUNEL and Comet assay. Elucidation of molecular mechanism through immunoblot and further validation of the drug effect through in vivo approaches. Results: Initial in vitro anti-proliferative screening of Compounds DPA (7a-t) against multiple cancer cell lines identified Compound DPA (7n) as a potent cytotoxic molecule with IC Conclusions: Compound DPA (7n) emerged as a potent proapoptotic and anti-neoplastic agent by inhibiting ATM kinase activity both in vitro and in vivo. The conferring results ascertain that the drug could be developed as a new ATM kinase inhibitor with anti-cancer capacity.
MeSH term(s)	Acetamides/chemical synthesis ; Acetamides/pharmacology ; Animals ; Antineoplastic Agents/chemical synthesis ; Antineoplastic Agents/pharmacology ; Apoptosis ; Cell Line, Tumor ; DNA Damage ; DNA Repair ; Drug Delivery Systems ; Humans ; Mice ; Mice, Inbred BALB C ; Molecular Structure ; Neoplasms, Experimental/drug therapy ; Xenograft Model Antitumor Assays
Chemical Substances	Acetamides ; Antineoplastic Agents
Language	English
Publishing date	2021-06-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2186248-5
ISSN	1734-1140
ISSN	1734-1140
DOI	10.1007/s43440-021-00292-6
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Article: Antiproliferative pharmacophore azo-hydrazone analogue BT-1F exerts death signalling pathway targeting STAT3 in solid tumour.

Banumathi / Sherapura, Ankith / Malojirao, Vikas H / Zabiulla / Sharath, B S / Thirusangu, Prabhu / Mahmood, Riaz / Kumari, N Suchetha / Baliga, Shrinath M / Khanum, Shaukath Ara / Prabhakar, B T

Pharmacological reports : PR

2022 Volume 74, Issue 2, Page(s) 353–365

Abstract: Background: Anomalous activation of intra-cellular signalling cascades confers neoplastic properties on malignant cells. The JAK2/STAT3 proteins play a pivotal role in the pathogenesis of most of the solid malignancies. The over expression of STAT3 in ... ...

Abstract	Background: Anomalous activation of intra-cellular signalling cascades confers neoplastic properties on malignant cells. The JAK2/STAT3 proteins play a pivotal role in the pathogenesis of most of the solid malignancies. The over expression of STAT3 in these tumours results in an evasion of apoptosis and thereby pathogenesis. Hence, strategy to target STAT3 to regress tumour development is an emerging new concept. As an approach, anti-neoplastic drug, Azo-hydrozone analogue, BT-1F with potential anti-proliferative effect was evaluated to demonstrate its capacity to counteract STAT3 signal with mechanistic approach. Methods: Cell based screening for cytotoxicity was performed through MTT, LDH and Trypan blue. The BT-1F induced anti-clonogenic property by clonogenic assay. The apoptotic capacity was examined by crystal violet staining, flow cytometry, Annexin-FITC, DAPI and TUNEL assay. The altered signalling events were studied using immunoblot. The drug-induced anti-tumour effect was evaluated in an in-vivo solid tumour model and molecular interaction was further validated by in-silico studies. Results: The BT-1F exerts chemo-sensitivity specifically against EAC and A549 cells without altering its normal counterpart. The anti-proliferative/anti-clonogenic effect was due to the induction of apoptosis through inhibition of STAT3 Conclusion: Systemic validation of STAT3 target drug, BT-1F in in-vitro, in-silico and in-vivo models has promising strategy for solid cancer treatment.
MeSH term(s)	Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Hydrazones/pharmacology ; Janus Kinase 2/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Hydrazones ; STAT3 Transcription Factor ; Tumor Suppressor Protein p53 ; Janus Kinase 2 (EC 2.7.10.2)
Language	English
Publishing date	2022-01-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2186248-5
ISSN	1734-1140
ISSN	1734-1140
DOI	10.1007/s43440-021-00345-w
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Article ; Online: Anti-neoplastic pharmacophore benzophenone-1 coumarin (BP-1C) targets JAK2 to induce apoptosis in lung cancer.

Sherapura, Ankith / Malojirao, Vikas H / Thirusangu, Prabhu / Sharath, B S / Kandagalla, Shivananda / Vigneshwaran, V / Novak, Jurica / Ranganatha, Lakshmi / Ramachandra, Y L / Baliga, Shrinath M / Khanum, Shaukath Ara / Prabhakar, B T

Apoptosis : an international journal on programmed cell death

2021 Volume 27, Issue 1-2, Page(s) 49–69

Abstract: Reigning of the abnormal gene activation associated with survival signalling in lung cancer leads to the anomalous growth and therapeutic failure. Targeting specific cell survival signalling like JAK2/STAT3 nexus has become a major focus of investigation ...

Abstract	Reigning of the abnormal gene activation associated with survival signalling in lung cancer leads to the anomalous growth and therapeutic failure. Targeting specific cell survival signalling like JAK2/STAT3 nexus has become a major focus of investigation to establish a target specific treatment. The 2-bromobenzoyl-4-methylphenoxy-acetyl hydra acetyl Coumarin (BP-1C), is new anti-neoplastic agent with apoptosis inducing capacity. The current study was aimed to develop antitumor phramacophore, BP-1C as JAK2 specific inhibitor against lung neoplastic progression. The study validates and identifies the molecular targets of BP-1C induced cell death. Cell based screening against multiple cancer cell lines identified, lung adenocarcinoma as its specific target through promotion of apoptosis. The BP-1C is able to induce, specific hall marks of apoptosis and there by conferring anti-neoplastic activity. Validation of its molecular mechanism, identified, BP-1C specifically targets JAK2
MeSH term(s)	Apoptosis ; Benzophenones/pharmacology ; Cell Line, Tumor ; Cell Proliferation ; Coumarins/pharmacology ; Humans ; Janus Kinase 2/genetics ; Janus Kinase 2/metabolism ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; STAT3 Transcription Factor/metabolism
Chemical Substances	Benzophenones ; Coumarins ; STAT3 Transcription Factor ; JAK2 protein, human (EC 2.7.10.2) ; Janus Kinase 2 (EC 2.7.10.2)
Language	English
Publishing date	2021-11-27
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1452360-7
ISSN	1573-675X ; 1360-8185
ISSN (online)	1573-675X
ISSN	1360-8185
DOI	10.1007/s10495-021-01699-5
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Article ; Online: Synthesis and amelioration of inflammatory paw edema by novel benzophenone appended oxadiazole derivatives by exhibiting cyclooxygenase-2 antagonist activity.

Puttaswamy, Naveen / Malojiao, Vikas H / Mohammed, Yasser Hussein Eissa / Sherapura, Ankith / Prabhakar, B T / Khanum, Shaukath Ara

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2018 Volume 103, Page(s) 1446–1455

Abstract: Ten new 2(4-hydroxy-3-benzoyl) benzamide-5-phenyl-1,3,4-oxadiazole derivatives (10a-j) were synthesized by coupling 3-benzoyl-4-hydroxybenzoic acid (5) with 2-amino-5-phenyl-1,3,4-oxadiazoles (9a-j). The structures of these compounds were confirmed by IR, ...

Abstract	Ten new 2(4-hydroxy-3-benzoyl) benzamide-5-phenyl-1,3,4-oxadiazole derivatives (10a-j) were synthesized by coupling 3-benzoyl-4-hydroxybenzoic acid (5) with 2-amino-5-phenyl-1,3,4-oxadiazoles (9a-j). The structures of these compounds were confirmed by IR,
MeSH term(s)	Animals ; Benzophenones/chemical synthesis ; Benzophenones/chemistry ; Benzophenones/pharmacology ; Benzophenones/therapeutic use ; Chickens ; Cyclooxygenase 2/metabolism ; Cyclooxygenase 2 Inhibitors/pharmacology ; Cyclooxygenase 2 Inhibitors/therapeutic use ; Edema/complications ; Edema/drug therapy ; Edema/enzymology ; Humans ; Inflammation/complications ; Inflammation/drug therapy ; Inflammation/enzymology ; Male ; Neovascularization, Physiologic/drug effects ; Oxadiazoles/chemical synthesis ; Oxadiazoles/chemistry ; Oxadiazoles/pharmacology ; Oxadiazoles/therapeutic use ; Rats
Chemical Substances	Benzophenones ; Cyclooxygenase 2 Inhibitors ; Oxadiazoles ; benzophenone (701M4TTV9O) ; Cyclooxygenase 2 (EC 1.14.99.1)
Language	English
Publishing date	2018-05-07
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2018.04.167
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Article: Novel 1,3,4-oxadiazole Targets STAT3 Signaling to Induce Antitumor Effect in Lung Cancer.

Malojirao, Vikas H / Girimanchanaika, Swamy S / Shanmugam, Muthu K / Sherapura, Ankith / Dukanya / Metri, Prashant K / Vigneshwaran, Vellingiri / Chinnathambi, Arunachalam / Alharbi, Sulaiman Ali / Rangappa, Shobith / Mohan, Chakrabhavi Dhananjaya / Basappa / Prabhakar, Bettadathunga T / Rangappa, Kanchugarakoppal S

Biomedicines

2020 Volume 8, Issue 9

Abstract: Lung cancer is the leading type of malignancy in terms of occurrence and mortality in the global context. STAT3 is an oncogenic transcription factor that is persistently activated in many types of human malignancies, including lung cancer. In the present ...

Abstract	Lung cancer is the leading type of malignancy in terms of occurrence and mortality in the global context. STAT3 is an oncogenic transcription factor that is persistently activated in many types of human malignancies, including lung cancer. In the present report, new oxadiazole conjugated indazoles were synthesized and examined for their anticancer potential in a panel of cancer cell lines. Among the new compounds, 2-(3-(6-chloro-5-methylpyridin-3-yl)phenyl)-5-(1-methyl-1H-indazol-3-yl)-1,3,4-oxadiazole (CHK9) showed consistently good cytotoxicity towards lung cancer cells with IC
Language	English
Publishing date	2020-09-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines8090368
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