<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Kulkarni, Akshay S.</style></author><author><style face="normal" font="default" size="100%">Dash, Anshurekha</style></author><author><style face="normal" font="default" size="100%">Shingare, Rahul D.</style></author><author><style face="normal" font="default" size="100%">Chand, Jagdish</style></author><author><style face="normal" font="default" size="100%">Manhas, Diksha</style></author><author><style face="normal" font="default" size="100%">Singh, Aman</style></author><author><style face="normal" font="default" size="100%">Nandi, Utpal</style></author><author><style face="normal" font="default" size="100%">Goswami, Anindya</style></author><author><style face="normal" font="default" size="100%">Reddy, D. Srinivasa</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Identification of new modulator of DNA repairing pathways based on natural product (±)-peharmaline A</style></title><secondary-title><style face="normal" font="default" size="100%">Bioorganic &amp; Medicinal Chemistry</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">DNA damage</style></keyword><keyword><style  face="normal" font="default" size="100%">EMT</style></keyword><keyword><style  face="normal" font="default" size="100%">Pictet</style></keyword><keyword><style  face="normal" font="default" size="100%">Spengler reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">Structure-activity relationship</style></keyword><keyword><style  face="normal" font="default" size="100%">Total synthesis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2023</style></year><pub-dates><date><style  face="normal" font="default" size="100%">AUG</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">91</style></volume><pages><style face="normal" font="default" size="100%">117365</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;
	The complex heterogenic environment of tumour mass often leads to drug resistance and facilitate chemo insensitivity triggering more malignant phenotypes among cancer patients. Major DNA-damaging cancer drugs have been consistently proven unsuccessful in terms of elevating chemo-resistance. (&amp;amp; PLUSMN;)-peharmaline A, a hybrid natural product isolated from seeds of Peganum harmala L. possesses significant cytotoxic activities. Herein, we have described the design, and synthesis of a novel library of close and simplified analogues around the anticancer natural product (&amp;amp; PLUSMN;)-peharmaline A and investigated their cytotoxic activities, which led to the identification of three structurally simplified lead compounds exhibiting better potency than parent natural product. Among them, demethoxy analogue of peharmaline A was further investigated for its anticancer potential eliciting demethoxy analogue as potent DNA-damage inducing agent attenuating the expression of the proteins responsible for the DNA damage repair. Therefore, this demethoxy analogue warrants detailed investigations for the confirmations of the molecular mechanism-based studies responsible for its anticancer activity.&lt;/p&gt;
</style></abstract><work-type><style face="normal" font="default" size="100%">Article</style></work-type><custom3><style face="normal" font="default" size="100%">&lt;p&gt;
	Foreign&lt;/p&gt;
</style></custom3><custom4><style face="normal" font="default" size="100%">&lt;p&gt;
	3.5&lt;/p&gt;
</style></custom4></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Saini, Sapna</style></author><author><style face="normal" font="default" size="100%">Reddy, G. Lakshma</style></author><author><style face="normal" font="default" size="100%">Gangwar, Anjali</style></author><author><style face="normal" font="default" size="100%">Kour, Harpreet</style></author><author><style face="normal" font="default" size="100%">Nadre, Gajanan G.</style></author><author><style face="normal" font="default" size="100%">Pandian, Ramajayan</style></author><author><style face="normal" font="default" size="100%">Pal, Sunny</style></author><author><style face="normal" font="default" size="100%">Nandi, Utpal</style></author><author><style face="normal" font="default" size="100%">Sharma, Rashmi</style></author><author><style face="normal" font="default" size="100%">Sawant, Sanghapal D.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Discovery and biological evaluation of nitrofuranyl-pyrazolopyrimidine hybrid conjugates as potent antimicrobial agents targeting Staphylococcus aureus and methicillin-resistant S. aureus</style></title><secondary-title><style face="normal" font="default" size="100%">RSC Medicinal Chemistry</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2025</style></year><pub-dates><date><style  face="normal" font="default" size="100%">MAR</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">1304-1328</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;
	Nitrofuran and pyrazolopyrimidine-based compounds possess a broad antimicrobial spectrum including Gram-positive and Gram-negative bacteria. In the present work, a series of conjugates of these scaffolds was synthesized and evaluated for antimicrobial activity against Staphylococcus aureus and methicillin-resistant S. aureus (MRSA). Many compounds showed MIC values of &amp;lt;= 2 mu g ml-1, with compound 35 demonstrating excellent activity (MICs: 0.7 and 0.15 mu g ml-1 against S. aureus and MRSA, respectively) and safety up to 50 mu g ml-1 in HepG2 cells. Compound 35 also exhibited no hemolytic activity, biofilm eradication, and effectiveness against efflux-pump-overexpressing strains (NorA, TetK, MsrA) without resistance development. It showed synergistic effects with vancomycin (S. aureus) and rifampicin (MRSA). Mechanistic studies revealed that compound 35 exhibits good membrane-targeting abilities, as evidenced by DAPI/PI staining and scanning electron microscopy (SEM). In an intracellular model, it reduced bacterial load efficiently in both S. aureus and MRSA strains. With a strong in vitro profile, compound 35 demonstrated favorable oral pharmacokinetics at 30 mg kg-1 and potent in vivo anti-MRSA activity, highlighting its potential against antibiotic-resistant infections.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><work-type><style face="normal" font="default" size="100%">Article</style></work-type><custom3><style face="normal" font="default" size="100%">&lt;p&gt;
	Foreign&lt;/p&gt;
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	4.1&lt;/p&gt;
</style></custom4></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Dash, Anshurekha</style></author><author><style face="normal" font="default" size="100%">Kulkarni, Akshay S.</style></author><author><style face="normal" font="default" size="100%">Irshad, Faisal</style></author><author><style face="normal" font="default" size="100%">Masal, Dattatraya P.</style></author><author><style face="normal" font="default" size="100%">Manhas, Diksha</style></author><author><style face="normal" font="default" size="100%">Nandi, Utpal</style></author><author><style face="normal" font="default" size="100%">Reddy, D. Srinivasa</style></author><author><style face="normal" font="default" size="100%">Goswami, Anindya</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Interplay between genotoxic stress and STING activation in cellular senescence and inflammatory responses</style></title><secondary-title><style face="normal" font="default" size="100%">International Immunopharmacology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">ATM</style></keyword><keyword><style  face="normal" font="default" size="100%">IL-6</style></keyword><keyword><style  face="normal" font="default" size="100%">Peharmaline</style></keyword><keyword><style  face="normal" font="default" size="100%">Senescence</style></keyword><keyword><style  face="normal" font="default" size="100%">STING</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2025</style></year><pub-dates><date><style  face="normal" font="default" size="100%">OCT</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">164</style></volume><pages><style face="normal" font="default" size="100%">115371</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;
	STING pathway is activated by endogenous or exogenous DNA damage and is known to trigger cell-intrinsic innate immunity. In this study, we demonstrated that the Peharmaline analog NDS101781 is a potent genotoxic molecule to trigger cellular senescence via innate immune-responsive STING activation. We found NDS101781 consistently modulated the expression of DDR markers including gamma-H2AX, Rad51, PARP1, ATM and MRE11 in breast cancer cells with concomitant amplification in the hallmarks of senescence along with STING signaling mediators which is intricately involved in NDS101781-mediated senescence activation as evidenced by significant reduction in the senescent population in si-TMEM173-transfected cells. In vitro findings proclaimed that STING activation by NDS101781 is crucial for p21-mediated senescence augmentation, a process regulated by ATM and p53 via a pathway independent of cGAS. Although STING is activated by both canonical and non-canonical manner, our mechanistic findings indicated that ATM played a crucial role in early activation of NDS101781 driven STING signaling via p53 activation and stimulation of pTBK1, NF-kappa B, and p-IRF3, through a non-canonical cascade in cGAS-independent mechanism. The results also indicated that interference of canonical and non-canonical STING activation, responsible for NF-kappa B stimulation leading to IL-6 generation. Intriguingly, the inhibition of ATM diminished senescence hallmarks; however, suppression of ATM as well as p21 neutralization triggered apoptotic cascade and thus regulating the SASP factors. However, transient knockdown of p21 moderately instigated the apoptotic mediators underscoring that NDS101781 mediated senescence induction delayed programmed cell death under intact p21 conditions. Moreover, pharmacokinetics of NDS101781 confirmed its excellent half-life in a preclinical model and in vivo studies confirmed that NDS101781 significantly inhibited tumor growth in a syngeneic aggressive 4T1-p53 breast cancer model.&lt;/p&gt;
</style></abstract><work-type><style face="normal" font="default" size="100%">Article</style></work-type><custom3><style face="normal" font="default" size="100%">&lt;p&gt;
	Foreign&lt;/p&gt;
</style></custom3><custom4><style face="normal" font="default" size="100%">&lt;p&gt;
	4.7&lt;/p&gt;
</style></custom4></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Kour, Dilpreet</style></author><author><style face="normal" font="default" size="100%">Khajuria, Parul</style></author><author><style face="normal" font="default" size="100%">Sharma, Kuhu</style></author><author><style face="normal" font="default" size="100%">Sharma, Alpa</style></author><author><style face="normal" font="default" size="100%">Sharma, Ankita</style></author><author><style face="normal" font="default" size="100%">Ali, Syed Mudassir</style></author><author><style face="normal" font="default" size="100%">Wazir, Priya</style></author><author><style face="normal" font="default" size="100%">Ramajayan, P.</style></author><author><style face="normal" font="default" size="100%">Sawant, Sanghapal D.</style></author><author><style face="normal" font="default" size="100%">Nandi, Utpal</style></author><author><style face="normal" font="default" size="100%">Ahmed, Zabeer</style></author><author><style face="normal" font="default" size="100%">Kumar, Ajay</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Isobavachalcone ameliorates Alzheimer disease pathology by autophagy-mediated clearance of amyloid beta and inhibition of NLRP3 inflammasome in primary astrocytes and 5x-FAD mice</style></title><secondary-title><style face="normal" font="default" size="100%">Frontiers in Pharmacology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Alzheimer disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Amyloid beta</style></keyword><keyword><style  face="normal" font="default" size="100%">Autophagy</style></keyword><keyword><style  face="normal" font="default" size="100%">isobavachalcone</style></keyword><keyword><style  face="normal" font="default" size="100%">neuroinflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">NLRP3 inflammasome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2025</style></year><pub-dates><date><style  face="normal" font="default" size="100%">MAR</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">1525364</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;
	Background and Aim Alzheimer's disease (AD) progresses with A beta plaque deposition and neuroinflammation. Given the complexity of AD pathology, single-target therapies have frequently failed in clinical trials. We hypothesized that a multitarget approach could yield better therapeutic outcomes. To this end, we identified isobavachalcone (IBC), a natural compound with dual pharmacological activity in reducing A beta plaques and neuroinflammation.Experimental Procedure Primary astrocytes were isolated from 3 to 4 days old C57BL/6J mice pups for in-vitro assays, while in-vivo studies were conducted on 5x-FAD mice. Protein alterations were evaluated using ELISA, western blotting, immunocytochemistry, and immunohistochemistry. Behavioral analyses included the radial arm maze, open field, and rotarod tests. Data from all in vitro and in vivo experiments were analyzed by using one-way ANOVA and post-hoc Bonferroni tests.Results In-vitro analyses in astrocytes demonstrated that IBC at 5 and 10 mu M concentrations induce AMPK phosphorylation through CAMKK2, promoting autophagy and inhibiting the NLRP3 inflammasome in primary astrocytes. IBC-treated astrocytes exhibited significant clearance of extracellular amyloid beta. Mechanistic studies highlighted autophagy as a key factor in reducing both NLRP3 inflammasome activity and A beta levels. Two months of treatment of 5x-FAD mice with IBC at 25 and 50 mg/kg significantly improved cognitive functions, as evidenced by enhanced memory and motor performance in behavioral tests. Subsequent brain tissue analysis revealed that IBC upregulated autophagic proteins to reduce the brain's amyloid beta levels, resulting in decreased expression of neuroinflammation markers.Conclusion IBC effectively ameliorates AD pathology through autophagy-mediated clearance of A beta and suppressing neuroinflammation in 5x-FAD mice.&lt;/p&gt;
</style></abstract><work-type><style face="normal" font="default" size="100%">Article</style></work-type><custom3><style face="normal" font="default" size="100%">&lt;p&gt;
	Foreign&lt;/p&gt;
</style></custom3><custom4><style face="normal" font="default" size="100%">&lt;p&gt;
	4.4&lt;/p&gt;
</style></custom4></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Kulkarni, Akshay S.</style></author><author><style face="normal" font="default" size="100%">Ramana, Sreenivasa Rao</style></author><author><style face="normal" font="default" size="100%">Nuthakki, Vijay K.</style></author><author><style face="normal" font="default" size="100%">Bhatt, Shipra</style></author><author><style face="normal" font="default" size="100%">Jamwal, Ashiya</style></author><author><style face="normal" font="default" size="100%">Nandawadekar, Laxman D.</style></author><author><style face="normal" font="default" size="100%">Jotshi, Anshika</style></author><author><style face="normal" font="default" size="100%">Kumar, Ajay</style></author><author><style face="normal" font="default" size="100%">Nandi, Utpal</style></author><author><style face="normal" font="default" size="100%">Bharate, Sandip B.</style></author><author><style face="normal" font="default" size="100%">Reddy, D. Srinivasa</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Silicon incorporated tacrine: design, synthesis, and evaluation of biological and pharmacokinetic parameters</style></title><secondary-title><style face="normal" font="default" size="100%">RSC Medicinal Chemistry</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2025</style></year><pub-dates><date><style  face="normal" font="default" size="100%">JUN</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">2603-2614</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;
	Tacrine, an orally bioavailable cholinesterase inhibitor, was previously used to treat Alzheimer's disease but was withdrawn due to hepatotoxicity. The unique structural features of tacrine have once again captured the interest of medicinal chemists. However, the blood-brain barrier (BBB) permeability hampered the development of the majority of its new analogs. Herein, we employed a silicon switch approach for improving the BBB permeability of CNS drugs with tacrine as a tool compound. The replacement of C2 methylene of tacrine with dimethyl silicon yielded `sila-tacrine' that inhibits acetylcholinesterase as well as butyrylcholinesterase with IC50 values of 3.18 and 6.09 mu M, respectively. Sila-tacrine competitively inhibits acetylcholinesterase while it is a non-competitive inhibitor of butyrylcholinesterase. The molecular docking results corroborated with the in vitro cholinesterase inhibition activity of tacrine vs. sila-tacrine. Sila-tacrine demonstrated metabolic stability in HLM and MLM and exhibited superior plasma exposure in an oral pharmacokinetic study in Swiss albino mice. However, tissue distribution studies revealed lower-than-expected brain levels due to efflux pump-mediated transport. This study offers a proof-of-concept for the silicon switch approach in improving the BBB permeability of CNS-active compounds.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><work-type><style face="normal" font="default" size="100%">Article</style></work-type><custom3><style face="normal" font="default" size="100%">&lt;p&gt;
	Foreign&lt;/p&gt;
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	4.1&lt;/p&gt;
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