Reduced melatonin levels linked to greater diabetes risk - Life Extension Update

In continuation of my update on Melatonin....

"Melatonin receptors have been found throughout the body in many tissues including pancreatic islet cells, reflecting the widespread effects of melatonin on physiological functions such as energy metabolism and the regulation of body weight," Ciaran McMullan and colleagues at Brigham and Women's Hospital noted in their introduction to the article. "Loss-of-function mutations in the melatonin receptor are associated with insulin resistance and type 2 diabetes. Additionally, in a cross-sectional analysis of persons without diabetes, lower nocturnal melatonin secretion was associated with increased insulin resistance."

The researchers matched 370 women who developed diabetes while enrolled in the Nurses' Health Study with 370 nondiabetic participants. Morning urine samples obtained upon enrollment in 2000 were analyzed for the ratio of 6-sulfoxymelatonin (the major metabolite of melatonin) to creatinine in order to estimate overnight melatonin secretion.

Women with diabetes had a 6-sulfatoxymelatonin to creatinine ratio that was significantly lower than that of the control group. Among those whose ratio was among the lowest of the participants, the adjusted risk of developing diabetes was more than twice that of women whose ratio was among the highest group.

"This is the first time that an independent association has been established between nocturnal melatonin secretion and type 2 diabetes risk," announced Dr McMullan, who is a researcher in the Renal Division and Kidney Clinical Research Institute at BWH. "Hopefully this study will prompt future research to examine what influences a person's melatonin secretion and what is melatonin's role in altering a person's glucose metabolism and risk of diabetes."

"It is interesting to postulate from these data, in combination with prior literature, whether there is a causal role for reduced melatonin secretion in diabetes risk," the authors remark. "Further studies are needed to determine whether increasing melatonin levels (endogenously via prolonged nighttime dark exposure or exogenously via supplementation) can increase insulin sensitivity and decrease the incidence of type 2 diabetes."

Ref : http://jama.jamanetwork.com/article.aspx?articleid=1674239

Reduced melatonin levels linked to greater diabetes risk - Life Extension Update

FDA Approves Invokana to Treat Type 2 Diabetes

In continuation of my update on Canagliflozin

We know that, Canagliflozin (Invokana) is drug for the treatment of type 2 diabetes developed by Johnson & Johnson. In March 2013,  canagliflozin became the first in a new class of drugs for diabetes treatment to be approved. It is an inhibitor of subtype 2 sodium-glucose transport protein (SGLT2), which is responsible for at least 90% of the glucose reabsorption in the kidney. Blocking this transporter causes blood glucose to be eliminated through the urine..

FDA Approves Invokana to Treat Type 2 Diabetes

Ganetespib Shows Potency Against Lung Cancer

In continuation of my update on Ganetespib

Ganetespib Shows Potency Against Lung Cancer

FDA Approves Stivarga for Advanced Gastrointestinal Stromal Tumors

In continuation of my update on Stivagra

We know that, Regorafenib (BAY 73-4506, commercial name Stivarga) is an oral multi-kinase inhibitor developed by Bayer which targets angiogenic, stromal and oncogenic receptor tyrosine kinase (RTK). Regorafenib shows anti-angiogenic activity due to its dual targeted VEGFR2-TIE2 tyrosine kinase inhibition. It is currently being studied as a potential treatment option in multiple tumor types.

Now...

FDA Approves Stivarga for Advanced Gastrointestinal Stromal Tumors

FDA Approves Tecfidera - a New Treatment for Multiple Sclerosis

We know that, Dimethyl fumarate (DMF) is the methyl ester of fumaric acid. DMF was initially recognized as a very effective hypoxic cellradiosensitizer. Later, DMF combined with three other fumaric acid esters (FAE) was licensed in Germany as oral therapy for psoriasis (Fumaderm). Other diseases, such as necrobiosis lipoidica, granuloma annulare, and sarcoidosis were also found to respond to treatment with DMF in case reports or small patient series. Recently, phase III clinical trials found that DMF (BG-12) successfully reduced relapse rate and time to progression of disability in multiple sclerosis. DMF is thought to haveimmunomodulatory properties without significant immunosuppression.

In a non-medical use, DMF was applied as a biocide in furniture or shoes to prevent growths of mold during storage or transport in a humid climate. However, due to incidences of allergic reactions after skin contact the European Union banned DMF in consumer products since 1998, and since January 2009 the import of products containing DMF was also banned...

Now...

FDA Approves Tecfidera - a New Treatment for Multiple Sclerosis

FDA Approves Kadcyla for Late-Stage Breast Cancer

We know that, Trastuzumab emtansine  in the United States, ado-trastuzumab emtansine, trade name Kadcyla) is anantibody-drug conjugate consisting of the monoclonal antibody trastuzumab (Herceptin) linked to the cytotoxic agentmertansine (DM1). Trastuzumab alone stops growth of cancer cells by binding to the HER2/neu receptor, whereas mertansine enters cells and destroys them by binding to tubulin. Because the monoclonal antibody targets HER2, and HER2 is only over-expressed in cancer cells, the conjugate delivers the toxin specifically to tumor cells.

In the EMILIA clinical trial of women with advanced HER2 positive breast cancer who were already resistant to trastuzumab alone, it improved survival by 5.8 months compared to the combination of lapatinib and capecitabine. Based on that trial, the U.S. Food and Drug Administration (FDA) approved marketing on February 22, 2013.

Trastuzumab emtansine was developed by Genentech. The planned cost is expected to be $9,800 a month, or $94,000 for a typical course of treatment..

Now....

FDA Approves Kadcyla for Late-Stage Breast Cancer

Warner Chilcott Announces FDA Approval of New Ulcerative Colitis Product Delzicol

We know that, Mesalazine , also known as mesalamine (USAN) or 5-aminosalicylic acid (5-ASA), is an anti-inflammatory drug used to treat inflammatory bowel disease, such as ulcerative colitis and mild-to-moderate Crohn's disease. Mesalazine is a bowel-specificaminosalicylate drug that acts locally in the gut and has its predominant actions there, thereby having few systemic side effects.

As a derivative of salicylic acid, mesalazine is also thought to be an antioxidant that traps free radicals, which are potentially damaging byproducts of metabolism

Warner Chilcott plc announced that the United States Food and Drug Administration (FDA) has approved its new 400 mg mesalamine product indicated for the treatment of ulcerative colitis. The product will be marketed as Delzicol (mesalamine) 400 mg delayed-release capsules. The Company anticipates that it will commercially launch Delzicol in March 2013.

Warner Chilcott Announces FDA Approval of New Ulcerative Colitis Product Delzicol

Takeda Receives FDA Approval for Kazano (alogliptin and metformin) for Type 2 Diabetes

Takeda Pharmaceuticals U.S.A., Inc. today announced that the United States (U.S.) Food and Drug Administration (FDA) has approved Kazano (alogliptin and metformin HCl) for the treatment of type 2 diabetes in adults as adjuncts to diet and exercise. 

Kazano contains alogliptin, a dipeptidyl peptidase-4 inhibitor (DPP-4i) that is designed to slow the inactivation of incretin hormones GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic peptide). Kazano combines alogliptin with metformin HCl, a widely used anti-diabetes medication, in a single tablet.

The most common adverse events (greater than or equal to 4%) reported with alogliptin include nasopharyngitis, headache and upper respiratory tract infection. Common adverse events (greater than or equal to 4%) reported with Kazano include upper respiratory tract infection, nasopharyngitis, diarrhea, hypertension, headache, back pain and urinary tract infection.

Takeda is committed to providing type 2 diabetes patients with treatment options that help address their needs, and is planning to commercially launch Kazano in the summer of 2013.

Takeda's consolidated financial statements for the 2012 fiscal year will not be impacted by the FDA approvals.

Takeda Receives FDA Approval for Kazano (alogliptin and metformin) for Type 2 Diabetes

FDA Approves Exjade to Remove Excess Iron in Patients with Genetic Blood Disorder

In continuation of my update on Deferasirox

We know that, Deferasirox (marketed as Exjade) is a rationally-designed oral iron chelator. Its main use is to reduce chronic iron overload in patients who are receiving long-term blood transfusions for conditions such as beta-thalassemia and other chronic anemias. It is the first oral medication approved in the USA for this purpose.

It was approved by the United States Food and Drug Administration (FDA) in November 2005. According to FDA (May 2007), renal failure and cytopenias have been reported in patients receiving deferasirox oral suspension tablets. It is approved in the European Union by the European Medicines Agency (EMA) for children 6 years and older for chronic iron overload from repeated blood transfusions.....

FDA Approves Exjade to Remove Excess Iron in Patients with Genetic Blood Disorder

Santarus Receives FDA Approval of Uceris (budesonide) for the Induction of Remission in Patients with Active, Mild to Moderate Ulcerative Colitis

In continuation of my update on Budesonide

We know that, Budesonide is a glucocorticoid steroid for the treatment of asthma and non-infectious rhinitis (including hay fever and other allergies), and for treatment and prevention of nasal polyposis. In addition, it is used for Crohn's disease (inflammatory bowel disease).

It is marketed by AstraZeneca as a nasal inhalant under the brand name Rhinocort (in Denmark, as Rhinosol), as an oral inhalant under the brand name Pulmicort (in Israel, Budicort), and as either an enema or a modified-release oral capsule under the brand name Entocort. It is also sold in combination with formoterol (Oxis) in a single inhaler, under the brand name Symbicort. In Brazil it is marketed by Eurofarma under the brand name Noex. Entocort EC is an oral capsule marketed in the United States by Prometheus Laboratories.

Santarus Receives FDA Approval of Uceris (budesonide) for the Induction of Remission in Patients with Active, Mild to Moderate Ulcerative Colitis

FDA Approves Sirturo to Treat Multi-Drug Resistant Tuberculosis

In continuation of my update on bedaquiline...

Sirturo is being approved under the FDA’s accelerated approval program, which allows the agency to approve a drug to treat a serious disease based on clinical data showing that the drug has an effect on a surrogate endpoint that is reasonably likely to predict a clinical benefit to patients. This program provides patients earlier access to promising new drugs while the company conducts additional studies to confirm the drug’s clinical benefit and safe use.

The FDA also granted Sirturo fast track designation, priority review and orphan-product designation. The drug demonstrated the potential to fill an unmet medical need, has the potential to provide safe and effective treatment where no satisfactory alternative therapy exists, and is intended to treat a rare disease, respectively.

Sirturo carries a Boxed Warning alerting patients and health care professionals that the drug can affect the heart’s electrical activity (QT prolongation), which could lead to an abnormal and potentially fatal heart rhythm. The Boxed Warning also notes deaths in patients treated with Sirturo. Nine patients who received Sirturo died compared with two patients who received placebo. Five of the deaths in the Sirturo group and all of the deaths in the placebo arm seemed to be related to tuberculosis, but no consistent reason for the deaths in the remaining Sirturo-treated patients could be identified.

Sirturo’s manufacturer, Janssen Therapeutics, will distribute the drug from a single source and will provide educational materials to help ensure the drug is used appropriately.

Sirturo’s safety and effectiveness were established in 440 patients in two Phase 2 clinical trials. Patients in the first trial were randomly assigned to be treated with Sirturo plus other drugs used to treat TB, or a placebo plus other drugs used to treat TB. All patients in the second trial, which is ongoing, received Sirturo plus other TB drugs. Both studies were designed to measure the length of time it took for a patient’s sputum to be free of M. tuberculosis (sputum culture conversion, or SCC).

FDA Approves Sirturo to Treat Multi-Drug Resistant Tuberculosis

FDA Approves Juxtapid - New Orphan Drug for Rare Cholesterol Disorder

In continuation of my update on lomitapide..

US FDA, Juxtapid (lomitapide) to reduce low-density lipoprotein (LDL) cholesterol, total cholesterol, apolipoprotein B, and non-high-density lipoprotein (non-HDL) cholesterol in patients with homozygous familial hypercholesterolemia (HoFH). Juxtapid is intended for use in combination with a low fat diet and other lipid-lowering treatments.

FDA Approves Juxtapid - New Orphan Drug for Rare Cholesterol Disorder

FDA Approves Adasuve (loxapine) Inhalation Powder for the Acute Treatment of Agitation Associated with Schizophrenia or Bipo...

In continuation of my update on adasuve

FDA Approves Adasuve (loxapine) Inhalation Powder for the Acute Treatment of Agitation Associated with Schizophrenia or Bipo...

Discovery could increase efficacy of promising cystic fibrosis drug

We know that, Ivacaftor (trade name Kalydeco, developed as VX-770) is a potentiator approved for patients with the G551D mutation of cystic fibrosis. Ivacaftor was developed by Vertex Pharmaceuticals in conjunction with the Cystic Fibrosis Foundation.

Cystic fibrosis is caused by any one of several defects in a protein, cystic fibrosis transmembrane conductance regulator, which regulates fluid flow within cells and affects the components of sweat, digestive fluids, and mucus. The defect, which is caused by a mutation in the individual's DNA, can be in any of several locations along the protein, each of which interferes with a different function of the protein. G551D is a standard amino acid abbreviation for a mutation in which the amino acid glycine (G) in position 551 is replaced with aspartic acid (D). G551D is characterized by a dysfunctional CFTR protein on the cell surface. In the case of G551D, the protein is trafficked to the correct area, the epithelial cell surface, but once there the protein cannot transport chloride through the channel. Ivacaftor, a CFTR potentiator, improves the transport of chloride through the ion channel by binding to the channels directly to induce a non-conventional mode of gating which in turn increases the probability that the channel is open.

Accidental discovery of a mutation in CFTR, the R532 mutation, allowed MU researchers to reveal a new "non-strict coupling" relationship that occurs between the consumption of ATP, a molecule that provides energy in the body, and the opening and closing of the CFTR. They argue that the new information uncovered about this mechanism that controls the opening and closing of the CFTR and the passage of ions through it could explain how and where the new cystic fibrosis treatment Kalydeco (Vx-770) works.

"To his credit, Dr. Hwang exploited the behavior of the CFTR mutants to demonstrate that CFTR's gate is not strictly coupled to the nucleotide binding engine (NBD) that binds and splits ATP [energy] to drive conformational changes that regulate chloride flow through the CFTR protein channel," said colleague David Sheppard, PhD, an associate professor in the School of Physiology and Pharmacology at the University of Bristol in Bristol, U.K. who did not participate in the study.

In their study, MU researchers were able to observe the effects of the cystic fibrosis drug Vx-770 on the recently discovered R352 mutation. They found that Vx-770 enhances the activity of the CFTR channel by exploiting this "non-coupling" mechanism, a conclusion also supported by experimental results with the wild-type CFTR protein.

"Traditionally, researchers have defined how energy is utilized and transferred in the CFTR as a 'strict coupling' mechanism, meaning that one ATP molecule opens CFTR's gate, ions pass through and the ATP molecule is hydrolyzed and then the gate closes," Hwang said. "In this new model, we argue that the CFTR uses energy from ATP hydrolysis to carry out its function of chloride flow, but this coupling mechanism is more plastic than we thought and therefore could be subjective to manipulations by drugs such as Vx-770."

CFTR is part of a family of thousands of active transporter proteins called ABC proteins. Although CFTR may share many structural features with its ABC "cousins," as Hwang calls them, it has been unclear as to whether CFTR and its cousins may work in a similar manner.

The new idea of how the CFTR utilizes ATP to carry out its function may bear a broader implication because of the evolutionary relationship between CFTR and other ABC transporter proteins. It opens up a wide variety of therapeutic possibilities for other common diseases, such as cancer, heart disease and diabetes, Hwang said, since many other ABC proteins play critical roles in those human illnesses.

"It's taken years for scientists to solve this particular puzzle about the CFTR protein," Hwang said. "Our recent study provides evidence that these ABC transporter proteins and CFTR, a chloride channel, are two peas in a pod. Mother nature employs the same structural framework with just a little bit of modification to do two totally different things. From a basic science perspective, it's a big deal.".....

Ref : http://www.pnas.org/content/110/11/4404.abstract?sid=3e58deab-1076-4255-b20b-73ff47495950

Discovery could increase efficacy of promising cystic fibrosis drug

Pain reliever shows anti-viral activity against flu

In continuation of my update on naproxen

New influenza vaccines must be developed annually, because the surface proteins they target mutate rapidly, the way cars used to get a whole new look every year. The researchers, led by Anny Slama-Schwok of the Institut National de la Recherche Agronomique, Jouy en Josas, France, found a much more stable, reliable target for anti-influenza activity. The so-called ribonucleoprotein complexes are necessary for replication, and the researchers realized they could target the nucleoprotein, preventing assembly of the complexes. Because of its vital function, the nucleoprotein is highly conserved, making it a good potential target for antiviral drugs.

The nucleoprotein's three dimensional structure, solved in 2006, provided the basis for searching for new drugs that could interfere with its action. The researchers did a virtual screening within the Sigma-Aldrich online catalog of biochemicals. That screening identified Naproxen, better known as the over-the-counter pain reliever Aleve, and as expected, it bound to the nucleoprotein, and impeded RNA binding, says Slama-Schwok. In further testing, it reduced the viral load in cells infected with H1N1 and H3N2 influenza A virus, and in mice it demonstrated a therapeutic index against influenza A that was superior to that of any other anti-inflammatory drug.

Specifically, naproxen blocks the RNA binding groove of the nucleoprotein, preventing formation of the ribonucleoprotein complex, thus taking the vital nucleoproteins out of circulation. The researchers write that naproxen is a lead compound for drug development that could be improved by tweaking the molecule to boost its ability to bind to nucleoprotein.

As an already approved drug, naproxen could become a treatment against influenza relatively quickly, the researchers write. Its status as a non-steroidal anti-inflammatory drug (NSAID), which inhibits the COX-2 pathway, as well as an antiviral would boost its efficacy.

Ref : http://aac.asm.org/content/early/2013/02/26/AAC.02335-12.abstract?sid=e3391873-6ffe-4f2e-8737-685e5f2ca15f

Pain reliever shows anti-viral activity against flu

New chemo drug gentler on fertility, tougher on cancer

We know that, Arsenic trioxide is the inorganic compound with the formula As₂O₃. This commercially important oxide of arsenic is the main precursor to other arsenic compounds, including organoarsenic compounds. Approximately 50,000 tonnes are produced annually.Many applications are controversial given the high toxicity of arsenic compounds.

A Tiny Trojan Horse

The chemotherapy drug, arsenic trioxide, is packed into a very tiny Trojan horse called a nanobin. The nanobin consists of nano-size crystalline arsenic particles densely packed and encapsulated in a fat bubble. The fat bubble, a liposome, disguises the deadly cargo   half a million drug molecules.

"You have to wallop the tumor with a significant dose of arsenic but at the same time prevent exposure to normal tissue from the drug," said O'Halloran. The fat bubble is hundreds of times smaller than the average human cell. It is the perfect size to stealthily slip through holes in the leaky blood vessels that rapidly grow to feed tumors. The local environment of the tumor is often slightly acid; it is this acid that causes the nanobin to release its drug cargo and deliver a highly effective dose of arsenic where it is needed.

The scientists show this approach to packaging and delivering the active drug has the desired effect on the tumor cells but prevents damage to ovarian tissue, follicles or eggs.

While the drug is gentle on fertility, it is ferocious on cancer. When tested against lymphoma, it was more potent than the drug in its traditional free form.

"The drug was designed to maximize its effectiveness but reduce fertotoxicity," said O'Halloran, also the Morrison Professor of Chemistry in the Weinberg College of Arts and Sciences at Northwestern. "Many cancer drugs cause sterilization, that's why the reproductive tract is really important to focus on in the new stages of drug design. Other body systems get better when people stop taking the drug, but fertility you can't recover."

Arsenic trioxide was approved a few years ago for treating some types of blood cancers such as leukemia in humans, but O'Halloran thinks the arsenic trioxide nanobins can be used against breast cancer and other solid tumors. In his previously published preclinical research, nanobins were effective in reducing tumor growth in triple-negative breast cancer, which often doesn't respond well to traditional chemotherapy and has a poor survival rate.

Quick Test For Fertility Toxicity

Woodruff was able to show early effects of the drug on fertility by using an in vitro follicle culture and a quick, simple new test she developed. She compared the fertotoxicity of the nanobin and free drug and found the nanobin was much less toxic to female fertility than the free drug in the experimental model.

"The system can be adapted very easily for any cancer drug under development to get an early peek under the tent,"said Woodruff, also the Thomas J. Watkins Memorial Professor of Obstetrics and Gynecology at Feinberg. "As this new drug goes forward in development, we can say this is a good drug for young female cancer patients who are concerned about fertility."

The information gained from the toxicity test will help inform the treatment decisions of oncologists and their young female cancer patients to improve their chances of creating a future family.

"They may prescribe less toxic drug regimens or refer them to specialists in fertility preservation," Woodruff said...

Ref : http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0058491

New chemo drug gentler on fertility, tougher on cancer

Positive results from Affinium Pharmaceuticals' Phase 2a clinical trial of AFN-1252 in ABSSSI

We know that, AFN-1252, is a selective inhibitor of Staphylococcus aureus enoyl-acyl carrier protein reductase (FabI), which is involved in fatty acid biosynthesis. 

Now, Affinium Pharmaceuticals announced today that its Phase 2a clinical trial evaluating oral AFN-1252   in acute bacterial skin & skin structure infections (ABSSSI) demonstrated excellent efficacy and safety data, marking a significant proof-of-concept milestone for Affinium's first-in-class, novel antibiotic targeted against bacterial fatty acid biosynthesis inhibition (FabI inhibitors).

A clinical study in 103 patients from 18 centers in the USA and Canada confirms excellent efficacy, safety and tolerability of 200 mg of oral AFN-1252 dosed twice daily for 5-14 days in patients with acute bacterial skin and skin structure infections (ABSSSI) due to Staphylococcus". Patients were recruited from outpatient or emergency room settings.   The enrolled patients had a variety of skin infections of ≥ 75 cm² in size, including severe abscesses (38%), cellulitis (27%), and wound infections (35%).  Investigators had the option of adding a second antibiotic to cover other potential pathogens or admitting the patient into the hospital. The vast majority of the patients were treated with oral AFN-1252 as monotherapy in the outpatient setting based on the suspicion of staphylococci from the clinical presentation and pretreatment Gram stain.  This study fully utilized recent FDA guidances for clinical trials in ABSSSI, including both entry and efficacy criteria.

Positive results from Affinium Pharmaceuticals' Phase 2a clinical trial of AFN-1252 in ABSSSI

Clinical Trials Move to the Petri Dish

In continuation of my update on azithromycinZithromax ....

The common antibiotic Zithromax received a new warning label from the U.S. Food and Drug Administration indicating it could cause dangerous arrhythmias in people with pre-existing heart conditions. Now, researchers at the Stanford University School of Medicine describe a “clinical trial in a dish” using patient-specific induced pluripotent stem, or iPS, cells to predict whether a drug will dangerously affect the heart’s function. The technique may be more accurate than the current in vitro drug-safety screening assays used by pharmaceutical companies, say the researchers, and may better protect patients from deadly side effects of common medications.

The technique allows scientists for the first time to test drugs directly on cells with mutations that cause hereditary cardiac diseases, rather than on the genetically modified human embryonic kidney cells or the Chinese hamster ovarian cells currently being used to detect cardiac toxicity.

The use of patient-specific iPS cells may help drug designers winnow heart-safe medications from those like the blockbuster anti-inflammatory drug Vioxx, which was withdrawn from the market because of unanticipated adverse cardiovascular events. It may also allow clinicians to identify sub-groups of patients, such as those with certain types of cardiac conditions, who should not be given certain drugs.

“Right now, the first time any drug sees a human heart cell is in a phase-1 clinical trial,” said Andrew Lee, a Stanford medical student and one of three lead authors of the study. “If adverse effects are seen, it can result in patient deaths, as in the case of the anti-inflammatory drug Vioxx or with cisapride, a drug previously used to treat digestive problems in people with diabetes. Right now, there are really no systematic studies to identify those people who are at risk.” Lee works in the laboratory of Joseph Wu, MD, PhD, who co-directs the Stanford Cardiovascular Institute, where the research was conducted.

The researchers anticipate that the technique, if adopted, could save millions of dollars and thousands of lives by streamlining the drug-testing process and increasing its sensitivity.

Clinical Trials Move to the Petri Dish

Soybeans can prevent cancer

Soybean meal is a bi-product following oil extraction from soybean seeds. It is rich in protein, which usually makes up around 40% of the nutritional components of the seeds and dependent on the line, and can also contain high oleic acid (a monounsaturated omega-9 fatty acid).

The study looked at the role soybeans could have in the prevention of cancer. Using a variety of soybean lines which were high in oleic acid and protein, the researchers looked to monitor bioactivity between the peptides derived from the meals of soybean and various types of human cancer cells.

The study showed that peptides derived from soybean meal significantly inhibited cell growth by 73% for colon cancer, 70% for liver cancer and 68% for lung cancer cells using human cell lines. This shows that the selected high oleic acid soybean lines could have a potential nutraceutical affect in helping to reduce the growth of several types of cancer cells.

Soybeans can prevent cancer

New class of anti-malarial compounds discovered

A group of researchers from 16 institutions around the world has identified a new class of anti-malarial compounds that target multiple stages of the malaria parasite's life cycle  These compounds could potentially be developed into drugs that treat and prevent malaria infection. Known as 4-(1H)-quinolone-3-diarylethers, the candidate anti-malarials are derived from a compound called endochin that effectively treats malaria in birds. When tested in the laboratory and in mice, the compounds demonstrated strong activity againstPlasmodium falciparum and Plasmodium vivax, the two parasites that cause most human cases of malaria. Transmitted via a mosquito bite, malaria causes cycles of chills, fever and fatigue, and is responsible for roughly 660,000 deaths per year, according to the World Health Organization. New drugs are needed because of the emergence of malaria-inducing parasites that are resistant to existing medications.

Of the 4-(1H)-quinolones, the researchers focused their efforts on the compound ELQ-300, which inhibited malaria parasites during the erythrocytic stage, when they cause symptoms in humans; as well as during the gametocyte and developmental stages in the mosquito, when the parasites are transmitted. In addition, when ELQ-300 was administered to mice infected with the Plasmodium species that cause malaria in mice, the infection was cured. The study results also suggested that the compound could be adapted into a once-daily dose in humans and would be slow to engender resistance. The researchers are currently proceeding with preclinical development of ELQ-300 (see the structure below).

Ref :1.  http://www.niaid.nih.gov/news/newsreleases/2013/Pages/ELQ300.aspx
2. http://stm.sciencemag.org/content/5/177/177ra37.short?rss=1

New class of anti-malarial compounds discovered

Drug treatment corrects autism symptoms in mouse model

The researchers tested suramin,  a well-known inhibitor of purinergic signaling used medically for the treatment of African sleeping sickness since shortly after it was synthesized in 1916 -- in mice. They found that this APT mediator corrected autism-like symptoms in the animal model, even if the treatment was started well after the onset of symptoms. The drug restored 17 types of multi-symptom abnormalities including normalizing brain synapse structure, cell-to-cell signaling, social behavior, motor coordination and normalizing mitochondrial metabolism.

"The striking effectiveness shown in this study using APT to 'reprogram' the cell danger response and reduce inflammation showcases an opportunity to develop a completely new class of anti-inflammatory drugs to treat autism and several other disorders," Naviaux said.

Ref : http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0057380

 Drug treatment corrects autism symptoms in mouse model