About the school


The School of Pharmacy at the Hebrew University, one of the world leaders in pharmacist training and basic research in the pharmaceutical sciences, was established in 1953.
The school prepares its graduates to practice the pharmacy profession, provides them with a scientific and professional foundation, and offers higher studies in pharmacology, medicinal chemistry and pharmacy sciences (M.Sc. and Ph.D.), as well as doctoral studies in clinical pharmacy (Pharm.D.).
Graduates of the school are integrated in community pharmacy (community pharmacies, private and institutional), clinical pharmacy (hospitals and health funds), the pharmaceutical industry, the biological, chemical and biotechnology industries, the pharmacy administration and science and research institutions in Israel and abroad.
The school conducts extensive scientific research in the fields of pharmaceutical sciences and life sciences, and dozens of articles are published each year in the leading press in the world of science.
The School of Pharmacy is part of the Faculty of Medicine, located on the Ein Kerem campus of the Hebrew University and works closely with physicians and researchers from Hadassah Hospital.
 

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Recent Publications

Aparna Anand, Abhinay Sharma, Miriam Ravins, Debabrata Biswas, Poornima Ambalavanan, Kimberly Xuan Zhen Lim, Rachel Ying Min Tan, Atul Kumar Johri, Boaz Tirosh, and Emanuel Hanski. 2021. “Unfolded protein response inhibitors cure group A streptococcal necrotizing fasciitis by modulating host asparagine.” Science Translational Medicine, 13, 605, Pp. eabd7465. Abstract
Group A streptococcus (GAS) is among the top 10 causes of mortality from an infectious disease, producing mild to invasive life-threatening manifestations. Necrotizing fasciitis (NF) is characterized by a rapid GAS spread into fascial planes followed by extensive tissue destruction. Despite prompt treatments of antibiotic administration and tissue debridement, mortality from NF is still high. Moreover, there is no effective vaccine against GAS, and early diagnosis of NF is problematic because its clinical presentations are not specific. Thus, there is a genuine need for effective treatments against GAS NF. Previously, we reported that GAS induces endoplasmic reticulum (ER) stress to gain asparagine from the host. Here, we demonstrate that GAS-mediated asparagine induction and release occur through the PERK-eIF2$\alpha$-ATF4 branch of the unfolded protein response. Inhibitors of PERK or integrated stress response (ISR) blocked the formation and release of asparagine by infected mammalian cells, and exogenously added asparagine overcame this inhibition. Moreover, in a murine model of NF, we show that the inhibitors minimized mortality when mice were challenged with a lethal dose of GAS and reduced bacterial counts and lesion size when mice were challenged with a sublethal dose. Immunohistopathology studies demonstrated that PERK/ISR inhibitors protected mice by enabling neutrophil infiltration into GAS-infected fascia and reducing the pro-inflammatory response that causes tissue damage. Inhibitor treatment was also effective in mice when started at 12 hours after infection. We conclude that host metabolic alteration induced by PERK or ISR inhibitors is a promising therapeutic strategy to treat highly invasive GAS infections.
Batya Isaacson, Maya Baron, Rachel Yamin, Gilad Bachrach, Francesca Levi-Schaffer, Zvi Granot, and Ofer Mandelboim. 2021. “The inhibitory receptor CD300a is essential for neutrophil-mediated clearance of urinary tract infection in mice.” European Journal of Immunology, 51, 9, Pp. 2218–2224. Abstract
Neutrophils play a crucial role in immune defense against and clearance of uropathogenic Escherichia coli (UPEC)-mediated urinary tract infection, the most common bacterial infection in healthy humans. CD300a is an inhibitory receptor that binds phosphatidylserine and phosphatidylethanolamine, presented on the membranes of apoptotic cells. CD300a binding to phosphatidylserine and phosphatidylethanolamine, also known as the “eat me” signal, mediates immune tolerance to dying cells. Here, we demonstrate for the first time that CD300a plays an important role in the neutrophil-mediated immune response to UPEC-induced urinary tract infection. We show that CD300a-deficient neutrophils have impaired phagocytic abilities and despite their increased accumulation at the site of infection, they are unable to reduce bacterial burden in the bladder, which results in significant exacerbation of infection and worse host outcome. Finally, we demonstrate that UPEC's pore forming toxin $\alpha$-hemolysin induces upregulation of the CD300a ligand on infected bladder epithelial cells, signaling to neutrophils to be cleared.
Awanish Kumar and Abraham J. Domb. 2021. “Polymerization Enhancers for Cyanoacrylate Skin Adhesive.” Macromolecular Bioscience. Abstract
Cyanoacrylate glues are a renowned synthetic tissue sealant that cures rapidly through polymerization at room temperature, felicitating medical glues to treat skin wounds and surgical openings. Despite a wide range of cyanoacrylates available, only 2-octyl cyanoacrylates (OCA) provides the best biocompatibility. In this study, the polymerization and adhesive properties of 2-octyl cyanoacrylates (OCA) are explored in the presence of a highly biocompatible and biochemically inert polymer, poly(ethylene glycol) polyhedral oligomeric silsesquioxane (PEG-POSS). The effect of PEG-POSS on the polymerization of OCA is examined on a plastic surface and over pig skin. A peel-test is performed to evaluate the strength of OCA adhesive properties between two pieces of pig skin samples. Additionally, thin films of OCA are prepared using different fillers and evaluated for tear test. The results reveal that when applied on the plastic or pig skin, PEG-POSS initiated polymerization in OCA yields a high molecular weight OCA polymer with much better adhesive properties compared to commercially available cyanoacrylate adhesives. The relative change in the molecular weights of OCA compared to commercially available cyanoacrylate bioadhesives such as Dermaflex is much higher. The pig skin peeling test shows that OCA needs higher peeling force than Dermaflex.
Aniv Mann Brukner, Sarah Billington, Mony Benifla, Tot Bui Nguyen, Hadas Han, Odeya Bennett, Tal Gilboa, Dana Blatch, Yakov Fellig, Olga Volkov, Jashvant D. Unadkat, Dana Ekstein, and Sara Eyal. 2021. “Abundance of P-glycoprotein and Breast Cancer Resistance Protein Measured by Targeted Proteomics in Human Epileptogenic Brain Tissue.” Molecular Pharmaceutics, 18, 6, Pp. 2263–2273. Abstract
Our goal was to measure the absolute differential abundance of key drug transporters in human epileptogenic brain tissue and to compare them between patients and at various distances from the epileptogenic zone within the same patient. Transporter protein abundance was quantified in brain tissue homogenates from patients who underwent epilepsy surgery, using targeted proteomics, and correlations with clinical and tissue characteristics were assessed. Fourteen brain samples (including four epileptogenic hippocampal samples) were collected from nine patients. Among the quantifiable drug transporters, the abundance (median, range) ranked: breast cancer resistance protein (ABCG2/BCRP; 0.55, 0.01-3.26 pmol/g tissue) > P-glycoprotein (ABCB1/MDR1; 0.30, 0.02-1.15 pmol/g tissue) > equilibrative nucleoside transporter 1 (SLC29A1/ENT1; 0.06, 0.001-0.35 pmol/g tissue). The ABCB1/ABCG2 ratio (mean 0.27, range 0.08-0.47) was comparable with literature values from nonepileptogenic brain tissue (mean 0.5-0.8). Transporter abundance was lower in the hippocampi than in the less epileptogenic neocortex of the same patients. ABCG2/BCRP and ABCB1/MDR1 expression strongly correlated with that of glucose transporter 1 (SLC2A1/GLUT1) (r = 0.97, p < 0.001; r = 0.90, p < 0.01, respectively). Low transporter abundance was found in patients with overt vascular pathology, whereas the highest abundance was seen in a sample with normally appearing blood vessels. In conclusion, drug transporter abundance highly varies across patients and between epileptogenic and less epileptogenic brain tissue of the same patient. The strong correlation in abundance of ABCB1/MDR1, ABCG2/BCRP, and SLC2A1/GLUT1 suggests variation in the content of the functional vasculature within the tissue samples. The epileptogenic tissue can be depleted of key drug transport mechanisms, warranting consideration when selecting treatments for patients with drug-resistant epilepsy.
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