Saturday, September 7, 2013

Alzheimer's 'missing link' found: Promising target for new drugs

Yale School of Medicine researchers have discovered a protein that is the missing link in the complicated chain of events that lead to Alzheimer's disease, they report in the Sept. 4 issue of the journal NeuronResearchers also found that blocking the protein with an existing drug can restore memory in mice with brain damage that mimics the disease.



Thursday, September 5, 2013

FDA Advisory Committee Unanimously Recommends Approval Of Bayer's Riociguat In Two Pulmonary Hypertension Indications

We know that, Riociguat is (BAY 63-2521) is a novel drug that is in clinical development by Bayer. It is a stimulator ofsoluble guanylate cyclase (sGC). At the moment Phase III clinical trials investigate the use of riociguat as a new approach to treat two forms of pulmonary hypertension (PH): chronic thromboembolic pulmonary hypertension (CTEPH) and pulmonary arterial hypertension (PAH). Riociguat constitutes the first drug of a novel class of sGC stimulators.


Monday, September 2, 2013

Drug used for blood cancers may stop spread of breast cancer cells

In continuation of my update on Decitabine

A drug used to treat blood cancers may also stop the spread of invasive breast cancer, researchers at Mayo Clinic in Florida have discovered. Their study, published online in Breast Cancer Research, found that in the lab and in animals, the drug decitabine turns on a gene coding for protein kinase D1 (PRKD1) that halts the ability of cancer cells to separate from a tumor and spread to distant organs.



Friday, August 30, 2013

Study: Type 2 diabetic patients treated with DPP-4 linagliptin experience reductions in blood glucose levels

Data published in The Lancet showed that elderly people with Type 2 Diabetes (T2D) treated for 24 weeks with the dipeptidyl peptidase-4 (DPP-4) inhibitor linagliptin, marketed by Boehringer Ingelheim and Eli Lilly and Company, experienced significant reductions in blood glucose levels (HbA1c) compared with those receiving placebo. In addition, the overall safety and tolerability profile of linagliptin was similar to placebo, with no significant difference in hypoglycaemia.

Wednesday, August 28, 2013

Watermelon juice relieves post-exercise muscle soreness


Encarna Aguayo and colleagues cite past research on watermelon juice's antioxidant properties and its potential to increase muscle protein and enhance athletic performance. But scientists had yet to explore the effectiveness of watermelon juice drinks enriched in L-citrulline. Aguayo's team set out to fill that gap in knowledge.


They tested natural watermelon juice, watermelon juice enriched in L-citrulline (ABOVE STRUCTURE) and a control drink containing no L-citrulline on volunteers an hour before exercise. Both the natural juice and the enriched juice relieved muscle soreness in the volunteers. L-citrulline in the natural juice (unpasteurized), however, seemed to be more bioavailable -- in a form the body could better use, the study found.

Watermelon juice relieves post-exercise muscle soreness

Tuesday, August 27, 2013

Combined therapy could repair and prevent damage in Duchenne muscular dystrophy, study suggests

Results from a clinical trial of eteplirsen, {RNA, [P-deoxy-P-(dimethylamino)](2',3'-dideoxy-2',3'-imino-2',3'-seco)(2'a→5')(C-m5U-   C-C-A-A-C-A-m5U-C-A-A-G-G-A-A-G-A-m5U-G-G-C-A-m5U-m5U-m5U-C-m5U-A-G),    5'-[P-[4-[[2-[2-(2-hydroxyethoxy) ethoxy]ethoxy] carbonyl]-1-piperazinyl]-N,N-   dimethylphosphonamidate]}  a drug designed to treat Duchenne muscular dystrophy, suggest that the therapy allows participants to walk farther than people treated with placebo and dramatically increases production of a protein vital to muscle growth and health. The study, led by a team in The Research Institute at Nationwide Children's Hospital, is the first of its kind to show these results from an exon-skipping drug -- a class of therapeutics that allows cells to skip over missing parts of the gene and produce protein naturally....


Monday, August 26, 2013

New approach in the treatment of breast cancer

Scientists at the MedUni Vienna, in collaboration with a working group led by Nancy Hynes at the University of Basel, have discovered a new approach in the treatment of breast cancer: an international team involving the Clinical Institute of Pathology at the MedUni Vienna has been able to demonstrate the activation of a receptor, the Ret protein (Rearranged during transfection), on the surface of breast cancer cells. Increased levels of this protein are associated with a lower likelihood of survival for breast cancer patients.


Read more about RET Inhibitors at : http://www.cancercommons.org/tag/ret-inhibitors/

Sunday, August 25, 2013

GLENMARK-A new way for a new world « New Drug Approvals


Undiminished zest..


“Every year we expect two more molecules to get into clinical trials,” says Saldanha, his zest undiminished by past failures. “In 2008, in a span of one or two quarters, our entire pipeline pretty much got wiped out, but we never lost our commitment and passion.” At that time its most advanced molecule, oglemilast, used for treating patients with chronic obstructive pulmonary disease, had to be abandoned when its Phase IIb trials produced unsatisfactory results. It also had to suspend clinical development of GRC 6211, a compound for treating osteoarthritis pain, because of side effects.



Friday, August 23, 2013

New treatment for brittle bone disease found

We know that, Risedronic acid (see structure) (INN) or risedronate sodium (USAN) is a bisphosphonate used to strengthen bone, treat or prevent osteoporosis, and treat Paget's disease of bone. It is produced and marketed by Warner ChilcottSanofi-Aventis, and in Japan by Takeda under the trade names ActonelAtelvia, and Benet. It is also available in a preparation that includes a calcium carbonate supplement, asActonel with Calcium.

Osteogenesis imperfecta (OI and sometimes known as brittle bone disease, or "Lobstein syndrome") is a congenital bone disorder. People with OI are born with defective connective tissue, or without the ability to make it, usually because of a deficiency ofType-I collagen. This deficiency arises from an amino acid substitution of glycine to bulkier amino acids in the collagen triple helixstructure. The larger amino acid side-chains create steric hindrance that creates a bulge in the collagen complex, which in turn influences both the molecular nanomechanics as well as the interaction between molecules, which are both compromised.[3] As a result, the body may respond by hydrolyzing the improper collagen structure. If the body does not destroy the improper collagen, the relationship between the collagen fibrils and hydroxyapatite crystals to form bone is altered, causing brittleness.[4] Another suggested disease mechanism is that the stress state within collagen fibrils is altered at the locations of mutations, where locally larger shear forces lead to rapid failure of fibrils even at moderate loads as the homogeneous stress state found in healthy collagen fibrils is lost.[3]These recent works suggest that OI must be understood as a multi-scale phenomenon, which involves mechanisms at the genetic, nano-, micro- and macro-level of tissues.