Mohali, India

NIPER Mohali is an Indian public Pharmacy research university, and a part of the seven schools, under India's Ministry of Chemicals and Fertilizers. The institute offers Masters and Doctoral degrees in pharmaceutical science. As an Institute of National Importance it plays an important role in the Human Resource Development for the ever growing Indian Pharmaceutical industry, which has been in the forefront of India’s science based industries with wide ranging capabilities in this important field of drug manufacture.The institute offers a 2 year PG degree course; MS in 9 disciplines and MBA . Wikipedia.


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Grant
Agency: Cordis | Branch: FP7 | Program: CP-SICA | Phase: HEALTH-2007-2.3.2-12 | Award Amount: 3.94M | Year: 2008

The increasing emergence of multidrug resistant strains and extensively drug resistant strains, the last one being virtually untreatable, urgently demand novel drugs for therapy of tuberculosis. This project has the aim of bringing together a number of research scientists with expertise in a broad range of disciplines, both from Europe and from India, covering the development field from chemistry to in vivo evaluation. The selected targets belong to either the group of targets from which some proof of concept already exist (mycolic acid synthesis and ATP synthase) either to the group of completely new targets that will be validated (thymidylate synthase, acyl-CoA carboxylase, DNA helicases). One alternative strategy to target the host cellular machinery to enhance bacterial killing is, likewise, included. The selected targets are covering fatty acid metabolism, nucleoside synthesis, energy generator, the survival of the microorganism in macrophages, the nucleic acids metabolism. The systems selected include those from which we expect to generate compounds active against replicating mycobacteria or to obtain compounds targeting latent infection. The application is divided in four scientific workpackages, including target validation, the interaction with the host cellular machinery, the design and synthesis of new inhibition and in vitro and in vivo screening of drug candidates and one management workpackage. A considerable part of the drug development and assessment against drug resistant Mycobacterium tuberculosis will be carried out by the Indian partners, one of which is an SME.


Mittal A.K.,National Institute of Pharmaceutical Education and Research | Chisti Y.,Massey University | Banerjee U.C.,National Institute of Pharmaceutical Education and Research
Biotechnology Advances | Year: 2013

Biomolecules present in plant extracts can be used to reduce metal ions to nanoparticles in a single-step green synthesis process. This biogenic reduction of metal ion to base metal is quite rapid, readily conducted at room temperature and pressure, and easily scaled up. Synthesis mediated by plant extracts is environmentally benign. The reducing agents involved include the various water soluble plant metabolites (e.g. alkaloids, phenolic compounds, terpenoids) and co-enzymes. Silver (Ag) and gold (Au) nanoparticles have been the particular focus of plant-based syntheses. Extracts of a diverse range of plant species have been successfully used in making nanoparticles. In addition to plant extracts, live plants can be used for the synthesis. Here we review the methods of making nanoparticles using plant extracts. Methods of particle characterization are reviewed and potential applications of the particles in medicine are discussed. © 2013 Elsevier Inc.


Karpe P.A.,National Institute of Pharmaceutical Education and Research | Tikoo K.,National Institute of Pharmaceutical Education and Research
Diabetes | Year: 2014

We have investigated the role of heat shock (HS) in preventing insulin resistance-induced endothelial dysfunction. To the best of our knowledge, we report here for the first time that insulin resistance inhibits vascular HS protein (HSP) 72 expression. HS treatment (41°C for 20 min) restored the HSP72 expression. High-fat diet (HFD)-fed, insulin-resistant rats show attenuated angiotensin (ANG)-(1-7)- induced vasodilator effect, endothelial nitric oxide synthase (eNOS) phosphorylation, AMP-activated protein kinase phosphorylation, and sirtuin 1 (SIRT1) expression. Interestingly, HS prevented this attenuation. We also provide the first evidence that HFD-fed rats show increased vascular DNA methyltransferase 1 (DNMT1) expression and that HS prevented this increase. Our data show that in HFD-fed rats HS prevented loss in the expression of ANG-(1-7) receptor Mas and ACE2, which were responsible for vascular complications. Further, the inhibition of eNOS (L-NG-nitro-L-arginine methyl ester), Mas (A-779), and SIRT1 (nicotinamide) prevented the favorable effects of HS. This suggests that HS augmented ANG-(1-7) signaling via the Mas/eNOS/SIRT1 pathway. Our study, for the first time, suggests that induction of intracellular HSP72 alters DNMT1 expression, and may function as an epigenetic regulator of SIRT1 and eNOS expression. We propose that induction of HSP72 is a novel approach to prevent insulin resistance-induced vascular complications. © 2014 by the American Diabetes Association..


Datusalia A.K.,National Institute of Pharmaceutical Education and Research | Sharma S.S.,National Institute of Pharmaceutical Education and Research
Molecular Neurobiology | Year: 2014

Chronic type 2 diabetes (T2D) causes cognitive deficits which are debilitating to the young as well as the older population. Glycogen synthase kinase-3β (GSK-3β) signaling has been reported to be impaired in insulin-resistant and T2D animal models. In this study, we have investigated the involvement of GSK-3β in cognitive deficits associated with T2D using SB216763, a GSK-3 β inhibitor. In high-fat diet-streptozotocin (HFD-STZ) model of T2D in rats, cognitive deficits appeared on the 15th week after induction of diabetes. Treatment with GSK-3β inhibitor SB216763 (i.p. daily for 3 weeks) reversed impaired cognitive performance in the Morris water maze, Y-maze, and passive avoidance tests. Administration of SB216763 also significantly improved acetylcholine esterase activity, GABA, and glutamate levels in the hippocampus and cortex of diabetic rats. Importantly, GSK-3β inhibition showed an increase in pGSK-3β and pCREB expression and reduction in pNF-κB-p65 expression in both hippocampus and cortex. Neuroinflammation was reduced by SB216763 in diabetic rats as evident from reduction in IL-6, TNF-α, COX-2, and inducible nitric oxide synthase levels. This study suggests that cognitive deficits associated with diabetes involved intricate compartmental interaction between transcription factors and neurotransmitter homeostasis/energy metabolism, and GSK-β might play a central role in diabetes-induced cognitive impairment. © 2014, Springer Science+Business Media New York.


Kaur J.,National Institute of Pharmaceutical Education and Research | Tikoo K.,National Institute of Pharmaceutical Education and Research
Biochimica et Biophysica Acta - Molecular Cell Research | Year: 2013

Gefitinib is an Epidermal Growth Factor Receptor (EGFR) tyrosine kinase inhibitor, approved for patients with non-small cell lung cancer (NSCLC). In this report we demonstrate that gefitinib loaded PLGA nanoparticles (GNPs), in comparison to gefitinib, exhibited higher anti-cancer activity on A549 lung carcinoma cells and A431 skin carcinoma cells. Increased inhibition of pEGFR in both the cell types explains its higher anti-cancer activity. Interestingly, gefitinib resistant, H1975 (T790M EGFR mutant) lung carcinoma cells was also found to be sensitive to GNPs. Our data shows that GNPs hyperacetylate histone H3 in these cells, either directly or indirectly, which may account for the augmented cell death. GNPs were proficient in activating histone acetyltransferases (p300/CBP), which in turn induces the expression of p21 and cell cycle arrest. Furthermore, inhibition of histone acetyltransferases by garcinol results in alleviation of cell death caused by GNPs. In addition to this, nuclear intrusion of GNPs results in the inhibition of NO production in nucleus, possibly through nuclear EGFR, which might be responsible for preventing cell proliferation in resistant cells. To best of our knowledge, we provide first evidence that GNPs potentiate cell death by activating p300/CBP histone acetyltransferases. © 2013 Elsevier B.V.


Jena G.,National Institute of Pharmaceutical Education and Research | Trivedi P.P.,National Institute of Pharmaceutical Education and Research
Inflammatory Bowel Diseases | Year: 2014

Ulcerative colitis (UC), an inflammatory bowel disease, affects many people across the globe, and its prevalence is increasing steadily. Inflammation and oxidative stress play a vital role in the perpetuation of inflammatory process and the subsequent DNA damage associated with the development of UC. UC induces not only local but also systemic damage, which involves the perturbation of multiple molecular pathways. Furthermore, UC leads to an increased risk of colorectal cancer, the third most common malignancy in humans. Most of the drugs used for the treatment of UC are unsatisfactory because they are generally mono-targeted, relatively ineffective and unaffordable for many people. Thus, agents that can target multiple molecular pathways and are less expensive have enormous potential to treat UC. Melatonin has beneficial effects against UC in experimental and clinical studies because of its ability to modulate several molecular pathways of inflammation, oxidative stress, fibrosis, and cellular injury. However, many novel targets are yet to be explored on which melatonin may act to exert its favorable effects in UC. It is time to explore improved intervention strategies with melatonin in UC on the basis of studies investigating different molecular targets using proteomic and genomic approaches. This review identifies various molecular targets for melatonin with the intent of providing novel strategies for combating UC and the associated extraintestinal manifestations of this debilitating disease. Copyright © 2014 Crohn's & Colitis Foundation of America, Inc.


Kaur J.,National Institute of Pharmaceutical Education and Research | Tikoo K.,National Institute of Pharmaceutical Education and Research
Oncogene | Year: 2015

Nanomedicine era is not far from its realization, but a major concern of targeted delivery still stands tall in its way. Herein we demonstrate the mechanism underlying the anticancer activity of an RNA aptamer (Apt) conjugated to gefitinib-loaded poly (lactic co-glycolic acid) nanoparticles (GNPs). Apt was selected through Cell-SELEX (systemic evolution of ligands by exponential enrichment) process against gefitinib-resistant H1975 lung cancer cells. The selected aptamer exhibited high specificity toward H1975 cells, both qualitatively as well as quantitatively. Software analysis using the MATCH tool predicted Ets1, a proto-oncoprotein, to be the target of the selected aptamer. Interestingly, the localization of identified aptamer varied in descending order of Ets1 expression, wherein maximum localization was observed in H1975 cells than in MDA-MB231, DU-145, H23, H460, A431, A549 and MCF-7 cells, and minimum in L132 cells. Furthermore, Apt-GNP bio-conjugate showed augmented anticancer activity specifically in Ets1-overexpressing cells. In addition, partial depletion of Ets1 in H1975 cells and overexpression of Ets1 in L132 cells reversed the targeting efficacy of the aptamer. Notably, a single intratumoral injection of the Apt-GNP bio-conjugate abrogated the growth of tumor in H1975 xenograft nude mice. Altogether, we present a pioneering platform, involving aptamers, which can be clinically used as a diagnostic marker for metastasis as well as an effective delivery system to escort the pharmaceutical cargo specifically to Ets1-overexpressing highly progressive tumors. © 2015 Macmillan Publishers Limited All rights reserved.


Roy S.R.,National Institute of Pharmaceutical Education and Research | Chakraborti A.K.,National Institute of Pharmaceutical Education and Research
Organic Letters | Year: 2010

Supramolecular assemblies formed by a relay of cooperative hydrogen bonds and charge-charge interactions have been identified/characterized by (+ve) ESI and MALDI-TOF-TOF MS and MS-MS studies during the aza-Michael reaction of amines with α,β-unsaturated carbonyl compounds in the presence of ionic liquids (ILs) digging out the role of catalysis by ILs, forming the basis of rational design/selection as organocatalysts, and offering a diagnostic model to predict/rationalize the selectivity of the aza-Michael reaction in a competitive environment. © 2010 American Chemical Society.


Patent
National Institute of Pharmaceutical Education and Research | Date: 2013-03-07

The present invention relates to nanocrystalline solid dispersion compositions having discrete particles, wherein each discrete particle comprises crystals of at least one pharmaceutical active; veterinary active; nutraceutical active dispersed in the matrix of at least one crystallization inducer and/or coexisting with crystals of crystallization inducer, optionally along with pharmaceutically acceptable excipients. The present invention also encompasses a novel one-step process for generation of nanocrystalline solid dispersions. The present invention is particularly of use for improving the dissolution of pharmaceutical actives, veterinary actives; nutraceutical actives exhibiting dissolution-limited bioavailability. Dissolution enhancement is because of the decreased crystallite size of the pharmaceutical active.


Jain V.,National Institute of Pharmaceutical Education and Research | Bharatam P.V.,National Institute of Pharmaceutical Education and Research
Nanoscale | Year: 2014

Nanoparticle based drug delivery systems are gaining popularity due to their wide spectrum advantages over traditional drug delivery systems; among them, dendrimeric nano-vectors are the most widely explored carriers for pharmaceutical and biomedical applications. The precise mechanism of encapsulation of drug molecules inside the dendritic matrix, delivery of drugs into specific cells, interactions of nano-formulation with biological targets and proteins, etc. present a substantial challenge to the scientific understanding of the subject. Computational methods complement experimental techniques in the design and optimization of drug delivery systems, thus minimizing the investment in drug design and development. Significant progress in computer simulations could facilitate an understanding of the precise mechanism of encapsulation of bioactive molecules and their delivery. This review summarizes the pharmacoinformatic studies spanning from quantum chemical calculations to coarse-grained simulations, aimed at providing better insight into dendrimer-drug interactions and the physicochemical parameters influencing the binding and release mechanism of drugs. © 2014 The Royal Society of Chemistry.

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