Volume 2, Number 4 - 6, October - December, 2012

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About the Cover

Omacetaxine Mepesuccinate to treat adults with chronic myelogenous leukemia
The U.S. Food and Drug Administration approved Synribo (omacetaxine mepesuccinate) to treat adults with chronic myelogenous leukemia (CML), a blood and bone marrow disease by October 26, 2012. Synribo blocks certain proteins that promote the development of cancerous cells. It is injected under the skin (subcutaneously) twice daily for 14 consecutive days over a 28-day cycle until white blood cell counts normalize (hematologic response). It is then administered twice daily for seven consecutive days over a 28-day cycle as long as patients continue to clinically benefit from therapy. It is the second drug approved to treat CML in the past two months. The mechanism of action has not been fully elucidated but includes inhibition of protein synthesis. It acts independently of direct Bcr-Abl binding to reduce protein levels of both the Bcr-Abl oncoprotein and Mcl-1 which inhibits apoptosis, in vitro. Bcr-Abl hybrid gene leads to over-production in the bone marrow of tyrosine kinase, an enzyme that causes too many stem cells to develop into white blood cells (granulocytes or blasts). It is the first protein synthesis inhibitor for the treatment of CML. The effectiveness was evaluated using a combined cohort of patients whose cancer progressed after previous treatment with two or more TKIs (tyrosine kinase inhibitors). The most common side effects include a low level of platelets in the blood (thrombocytopenia), low red blood cell count (anemia), a decrease in infection-fighting white blood cells (neutropenia) which may lead to infection and fever (febrile neutropenia), diarrhea, nausea, weakness and fatigue, injection site reaction, and a decrease in the number of lymphocytes in the blood (lymphopenia). It is marketed by Teva Pharmaceuticals USA. (Source: http://www.drugs.com/newdrugs/fda- approves-synribo-chronic-myelogenous-leukemia-3542.html)


Novel techniques in pharmacogenetic testing

Brithvi V

Pharmacogenetic tests play a major role in minimizing adverse drug reactions and enhancing optimal therapeutic response. The response to medication varies greatly between individuals, according to genetic constitution, age, sex, co-morbidities, environmental factors including diet and lifestyle (e.g. smoking and alcohol intake), and drug-related factors such as pharmacokinetic or pharmacodynamic drug-drug interactions. Databases on drug-drug interactions and the impact of pharmacogenetic polymorphisms and adverse drug reaction information systems will be helpful to guide clinicians in individualized treatment choices.

Discovery Pharmacy, 2012, 2(4), 3-4

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Ethno botany and antimicrobial activities of medicinal plants used for skin infections in Jimma, Ethiopia

Kothai S, Befirdu G

To document the valuable knowledge on herbal remedies to cure skin infections, ethnobotanical survey was conducted from October 2006 to November 2007 in Jimma an Ethiopian town. The survey identified nineteen plants and twenty two recipes to cure skin infections. Selected plants were evaluated for their antibacterial activity against Staphylococcus aureus and Streptococcus pyogenes commonly found in the wounds by agar well diffusion method.

Discovery Pharmacy, 2012, 2(4), 5-11

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G – Protein coupled receptors at a glimpse

Balasubramanian J

The vast majority of extracellular signaling molecules, like hormones and neurotransmitters, interact with a class of membranous receptors characterized by a uniform molecular architecture of seven transmembrane alpha-helices linked by extra- and intracelluar peptide loops.

Discovery Pharmacy, 2012, 2(5), 14-16

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Liraglutide: A Review on safety and efficacy of human glucagon – like peptide 1 analogue

Balasubramanian J, Narayanan N, Tamil selvan

Liraglutide, an analog of human GLP-1 and acts as a GLP-1 receptor agonist. The peptide precursor of liraglutide, produced by a process that includes expression of recombinant DNA in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting arginine for lysine at position 34. Liraglutide is made by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor. The molecular formula of liraglutide is C172H265N43O51 and the molecular weight is 3751.2 Daltons.

Discovery Pharmacy, 2012, 2(6), 19-21

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