Thursday, December 31, 2009
Mode of action : Phentermine, in doses clinically used, works on the hypothalamus portion of the brain to release norepinephrine, a neurotransmitter or chemical messenger that signals a fight-or-flight response, reducing hunger. Phentermine works outside the brain as well to release epinephrine or adrenaline causing fat cells to break down stored fat, but the principal basis of efficacy is hunger-reduction. At high doses, phentermine releases serotonin and dopamine as well, but such doses are never used in clinical medicine.
Tuesday, December 29, 2009
Gargling with green tea has already proved to prevent the onset of seasonal flu. It has become clear that catechin, a major type of polyphenol in green tea, plays a major role in prevention of flu infection, and that, among different types of catechin, EGCg displays the strongest antiviral activity. More interestingly, the researchers have conducted examinations to see if EGCg also shows antiviral activity against the new type of H1N1 virus, regardless of viral subtypes.
Solutions containing three types of viruses including the H1N1 virus were mixed with EGCg extracted from green tea. The mixture was added to cultured cells, which were thus infected. The cells were incubated for a set period of time, and the number of infected cells was counted. The concentration of EGCg at which virus infection was inhibited to 50% of the level of infection without EGCg was calculated.
The experiments showed that EGCg prevented flu virus infections at lower concentrations than Amantadine (a drug used to prevent and treat flu). A typical concentration of EGCg in green tea infused from a teapot is reported as 5,000-7,000 micromoles/L. Therefore, these results indicate that green tea diluted 1,000-fold or more is effective to halve infections by three types of viruses, including H1N1.
Those interested to know the details about green tea can visit the site.
Ref : http://www.itoen.co.jp/eng/corporate_info/index.html
Monday, December 28, 2009
As per the claim by the researchers, the compound exhibited more than 80 percent. Structure and activity of this class of furanones reveals that the exocyclic vinyl bromide conjugated with the carbonyl group is the most important structural element for fungal inhibition. Furthermore, gene expression analysis using DNA microarrays showed that 3 μg/mL of 4-bromo-5Z-(bromomethylene)-3-butylfuran-2-one (BF1) upregulated 32 C. albicans genes with functions of stress response, NADPH dehydrogenation, and small-molecule transport, and repressed 21 genes involved mainly in cell-wall maintenance.
Interestingly, only a small overlap is observed between the gene expression changes caused by the representative brominated furanone in this study and other antifungal drugs reported in literature. This result suggests that brominated furanones and other antifungal drugs may target different fungal proteins or genes.
The existence of such new targets provides an opportunity for developing new agents to control fungal pathogens which are resistant to currently available drugs.
The research team has also shown previously that these furanones inhibit bacterial biofilm formation; thus they may help control chronic infections where biofilms often appear, on surgical, dental and other implants. Hope broad spectrum of other potential capabilities make this class of compounds a new way to combat the microbes in the days to come...
Ref : http://springerlink.com/content/92735526v5013088/
Sunday, December 27, 2009
As per the claim by the authors, the negative intracellular redox potential reduces the platinum to release cisplatin, a Pt (II) compound, and two equivalents of DCA. By a unique mechanism, mitaplatin thereby attacks both nuclear DNA with cisplatin and mitochondria with DCA selectively in cancer cells. The cytotoxicity of mitaplatin in a variety of cancer cell lines equals or exceeds that of all known Pt (IV) compounds and is comparable to that of cisplatin.
Mitaplatin alters the mitochondrial membrane potential gradient of cancer cells, promoting apoptosis by releasing cytochrome c and translocating apoptosis inducing factor from mitochondria to the nucleus. Cisplatin formed upon cellular reduction of mitaplatin enters the nucleus and targets DNA to form 1,2-intrastrand d(GpG) cross-links characteristic of its own potency as an anticancer drug. These properties of mitaplatin are manifest in its ability to selectively kill cancer cells cocultured with normal fibroblasts and to partially overcome cisplatin resistance. Further studies like mice transplanted with human tissues are to be substantiated, in my opinion its a good achievement...
Ref : http://www.pnas.org/content/early/2009/12/09/0912276106.abstract?related-urls=yes&legid=pnas;0912276106v1
Saturday, December 26, 2009
The team has observed two effects on the cells: at a low dose cordycepin inhibits the uncontrolled growth and division of the cells and at high doses it stops cells from sticking together, which also inhibits growth. Both of these effects probably have the same underlying mechanism, which is that cordycepin interferes with how cells make proteins. At low doses cordycepin interferes with the production of mRNA, the molecule that gives instructions on how to assemble a protein. And at higher doses it has a direct impact on the making of proteins. More interestingly, the team has developed a very effective method that can be used to test new, more efficient or more stable versions of the drug in the Petri dish...
Ref : http://www.bbsrc.ac.uk/media/releases/2009/091223-new-insights-mushroom-derived-drug-for-cancer.html
Friday, December 25, 2009
Thursday, December 24, 2009
Wednesday, December 23, 2009
Tuesday, December 22, 2009
Fifteen of the 35 newly diagnosed patients in the open-label phase 2 portion of the study subsequently underwent autologous (using their own blood-forming stem cells) transplants, a standard treatment for multiple myeloma and did very well.
For the entire group, after a median 19.3 months of follow up, the median time-to-progression (TTP) of the disease, progression-free survival (PFS), and overall survival (OS) had not yet been reached, according to the presentation. The estimated TTP and PFS at one year are 76 percent, and the estimated one-year overall survival is 100 percent, the results showed.
Except for the main adverse effect, peripheral neuropathy (numbness or pain in the extremities), which typically cleared up after dosages were lowered and the treatment was completed.
The combination has now gone into large phase 3 clinical trials, and the researchers think that this regimen has the potential to be a new standard of treatment in multiple myeloma....
Monday, December 21, 2009
About apremilast :
Apremilast, is a member of a proprietary pipeline of novel small molecules with anti-inflammatory activities that inhibit the production of multiple proinflammatory mediators including, PDE-4, TNF-alpha, interleukin-2 (IL-2), interferon-gamma, leukotrienes, and nitric oxide synthase.
As per the claim by the company, 41% of patients treated with 30mg of oral apremilast BID achieved a PASI-75 after 16 weeks (p<0.001).
Ref : :http://ir.celgene.com/phoenix.zhtml?c=111960&p=irol-newsArticle&ID=1365878&highlight=
Sunday, December 20, 2009
The more interesting part of their research is that PAH patients had higher than normal blood levels of factors known to play central roles in the clogging of arteries as part of major diseases like atherosclerosis and hypertension, including angiopoietin-2 (Ang-2) and platelet derived growth factor. Treatment with treprostinil was associated with lowers levels of Ang-2.
Though the mode of action has to be established (relaxing muscles surrounding blood vessels for easier blood flow and turning off sticky ingredients that cause blood clots e.g. platelets) , its is a good achievement. Treprostinil-treated patients feel like they are breathing easier because their lung arteries, not the lungs themselves, are working more efficiently. Better understanding of the mechanisms involved may lead to refinements in drug design; for example, blocking the effects of Ang-2 to treat the disease (may be easier on patients than a continuous IV infusion). Though further studies are essential, its a good achievement and hope in the days to come people with PHT will definitely breathe a sigh of relief instead of breathlessnessssss.....
Source : http://www.urmc.rochester.edu/news/story/index.cfm?id=2711
Friday, December 18, 2009
Ref : http://newsroom.lilly.com/releasedetail.cfm?ReleaseID=429876
Thursday, December 17, 2009
Nilotinib, in the form of the hydrochloride monohydrate salt, is a tyrosine kinase inhibitor, approved as Tasigna in USA and the EU for drug - resistant chronic myelogenous leukemia (June 2006), resistant to treatment with imatinib (Gleevec), another tyrosine kinase inhibitor currently used as a first-line treatment.
As per the claim by the researchers, in the first head-to-head study of these two oral treatments as initial therapy for this life-threatening leukaemia, nilotinib demonstrated statistically significant improvement over imatinib in key measures of effectiveness used in the trial. The trial showed that at 12 months, significantly fewer patients on nilotinib 300mg twice-daily progressed from the initial chronic phase of the disease to the later accelerated or blast crisis phases than those on imatinib 400mg once-daily. This demonstrates that nilotinib provided significantly better control of the disease compared to imatinib.
95% of patients with CML have an abnormality known as the Philadelphia chromosome. This chromosome produces a type of protein called Bcr-Abl, which is responsible for the overproduction of the cancerous white blood cells that are the main feature in Ph+ CML. Nilotinib is a potent and selective inhibitor of the Bcr-Abl protein, thereby inhibiting the production of these cancerous cells.
Ref : http://www.novartis.com/newsroom/media-releases/en/2009/1359764.shtml
Wednesday, December 16, 2009
Now researchers from University of Virginia, Charlottesville, have come up with interesting info about the same drug. As per the claim by the researchers low doses of lidocaine given intravenously can help to control pain after common ambulatory surgery procedures. Intravenous lidocaine may offer a safe, inexpensive, and effective option for improving pain control after minimally invasive or minor surgery, reports the new study led by Dr Danja S. Groves of University of Virginia, Charlottesville. The results are surprising, because local anesthetics such as lidocaine are usually injected close to the nerve to numb the area for surgery. Though the anestheas (higher dose) are toxic, previous studies have found that that IV lidocaine injection is safe in small doses. Though the mode of action and anti inflammatory activity are still to be expalined, is a good achievement...
Ref : http://www.newswise.com/articles/view/559452/
Tuesday, December 15, 2009
Recently, researchers from Duke University Medical Center. Dr. Kimberly Blackwell have found more interesting results when they did try the combination of Trastuzumab (monoclonal antibody). As per the claim by the researchers, Lapatinib plus trastuzumab are significantly better than lapatinib alone in extending the lives of breast cancer patients whose tumors are HER2-positive.
Blackwell says, the combination targeted therapy gave patients more than a four-month survival advantage over those who took lapatinib alone. She says the findings may be the first step toward a chemotherapy-free future. This is the first time that a pair of targeted therapies has been shown to be superior to any intervention that paired a targeted therapy with a hormonal or chemotherapy based approach, she said. The interesting claim by the researchers trastuzumab binds to and blocks part of the HER2 growth factor that appears on the surface of some breast cancer cells while lapatinib binds to a second growth factor, EGFR, and part of HER2 that sits below the cell surface. It's sort of a double whammy, disabling the HER2 protein in two places instead of one......
Ref : http://www.dukehealth.org/health_library/news/targeted_therapy_prolongs_life_in_patients_with_her2_positive_breast_cancer
Monday, December 14, 2009
About monoclonal antibodies :
Ref : http://www.gene.com/gene/news/press-releases/display.do?method=detail&id=12487
Sunday, December 13, 2009
As per the claim by the researchers lead by Dr. Adam Brufsky , women who are on Medicare tend to go with tamoxifen because the cost of anastrozole puts them squarely in the donut hole of Medicare Part D, but once the cost barrier is removed there will likely be a mass switch to the aromatase inhibitor, which will necessitate the need for bone protection. More interestingly, in the same conference a research group lead by Rowan Chlebowski presented a study wherein "women who used bisphosphonates, had significantly fewer invasive breast cancers than women who did not use bisphosphonates. .......
Saturday, December 12, 2009
Higher antioxidant activity is reported for prenylchalcones than for prenyl flavanones in the Cu2+- mediated oxidation of LDL, suggesting a relation between structure and function. Also, many chalcones suppress tumor promotion more effectively than flavonoids themselves.
Quantities of xanthohumol found in Hop are to small to have any biological effects under normal consumption amounts. Some of the researchers also claims that it has got anti-HIV-1 activity too.
Now researchers from German Cancer Research Center, in Heidelberg, Germany, have come up with more interesting result, i.e., Xanthohumol of the male hormone testosterone.
Studies to date have shown that xanthohumol blocks the action of estrogen by binding to its receptor, which may lead to prevention of breast cancer. Since testosterone receptors act similarly to that of estrogen — by binding, then stimulating hormone-dependent effects, such as gene expression and cell growth — the researchers examined whether xanthohumol might not only block the effects of estrogen, but also of the male hormone androgen. Xanthohumol prevented the receptor from translocating to the cell nucleus, thus inhibiting its potential to stimulate the secretion of PSA and other hormone-dependent effects.
The interesting part of their research is the molecular modeling results, which showed that xanthohumol directly binds to the androgen receptor structure. The researchers suggest that this compound may have beneficial effects in animals — when they measured the anti-androgenic potential of xanthohumol in a rat model, they found that although xanthohumol was not able to prevent an increase in prostate weight after testosterone treatment, it could reduce testosterone-increased seminal vesicle weight.
As per the claim by the researchers the prostate weights were not changed, xanthohumol still reduced the effects of hormone signaling, such as gene expression, measured in the prostate tissue...
Ref : http://mct.aacrjournals.org/content/1/11/959.full
Friday, December 11, 2009
Ref : http://bloodjournal.hematologylibrary.org/cgi/content/full/110/9/3281/F1
Thursday, December 10, 2009
C. Jeffrey Brinker research group has determined that the very first stage of staph infection, when bacteria switch from a harmless to a virulent form, occurs in a single cell and that this individual process can be stopped by the application of a simple protein (as against the belief that, staph infections are caused by many bacterial cells that signal each other to emit toxins. The signaling process is called quorum sensing). The most significant results from the researchers are :
1. isolation of Staphylococcus aureus bacteria in individual (isolation of an individual bacterium
previously had been achieved only computationally);
2. demonstration of release of signaling peptides from a single cell, not a quorum &
3. introduction of an inexpensive, very low-density lipoprotein (VLDL) to bind to the
messenger peptide, they stopped the single cell from reprogramming itself.
One aspect of experimental rigor was the team's ability to organize living cells into a nanostructured matrix. The researchers has already done it with yeast, and just extended the process to bacteria. Researchers are optimistic about finding a mechanism to locate bacteria reprogramming in the body so that the antidote can be delivered in time. If they achieve what they are optimistic, so there will selectivity of targeting the bacteria (human gastro-intestinal system contains many useful bacteria) which in my opinion will be a remarkable feat....
Ref : http://www.nature.com/nchembio/journal/vaop/ncurrent/full/nchembio.264.html
Wednesday, December 9, 2009
The researchers confirmed lunasin's bioavailability in the human body by doing a third study in which men consumed 50 grams of soy protein--one soy milk shake and a serving of soy chili daily-for five days. Significant levels of the peptide in the participants' blood give us confidence that lunasin-rich soy foods can be important in providing these health benefits.
In the cancer study, de Mejia's group identified a key sequence of amino acids- arginine, glycine, and aspartic acid, (the RGD motif)--that triggered the death of leukemia cells by activating a protein called caspase-3. The scientists also verified lunasin's ability to inhibit topoisomerase 2, an enzyme that marks the development of cancer, and they were able to quantify the number of leukemia cells that were killed after treatment with lunasin in laboratory experiments.
More interesting out come of their study is lunasin's potential anti-inflammatory activity, (first time) they showed that lunasin blocked or reduced the activation of an important marker called NF-kappa-B, a link in the chain of biochemical events that cause inflammation. They also found statistically significant reductions in interleukin-1 and interleukin-6, both important players in the inflammatory process (the reduction in interleukin-6 was particularly strong). As per the claim by the group, although the high cost of obtaining lunasin from soy waste limits its use for nutritional interventions, soy flour does contain high concentrations of the peptide (depending on some genotype soy).
Its good see the diverse activities associated with Soy......
Source : http://pubs.acs.org/doi/abs/10.1021/jf803303k?prevSearch=Elvira%2Bde%2BMejia&searchHistoryKey=
Tuesday, December 8, 2009
Chaperone’s antimicrobial program focuses on development of peptide as well as small molecule hsp70 inhibitor drugs that block the effect of this important class of molecular “chaperones” whose role is to help mediate or respond to toxic misfolded proteins within bacteria. Inhibition of this critical bacterial protein has been proven to kill bacterial pathogens. Besides antimicrobials, the inhibition of hsp70 molecular chaperone proteins present in other cell-types has a range of therapeutic applications that are being investigated by the company.
Using sophisticated computerized molecular modeling techniques, proprietary high-throughput screening tools developed by Chaperone and other approaches, the company has significantly expanded its library of novel hsp70 inhibitor compounds including CHP-267 and CHP-281, just two of the many promising drug candidates from this highly promising family of small molecule inhibitors discovered by the Company. Chaperone is looking at hsp70 inhibitors as stand alone antimicrobial agents as well as in combination with other antimicrobials (e.g., Finafloxacin.HCl : see the structure -which is under phase II clinical trials). The company recently received a US Patent covering a method of significantly amplifying the effectiveness of other antimicrobials by combining their use with that of an hsp70 inhibitor. Combining a bacterial hsp70 inhibitor with another antimicrobial yields increased bacterial killing of clinically important pathogens and the potential for combination therapy.
Chaperone’s drug candidates have been proven effective against dangerous bacteria such as MRSA, acinetobacter, and vancomycin resistant enterococci. When combined with other antibiotics, Chaperone’s compounds stimulate powerful antibiotic synergy, providing superior efficacy even while using significantly lower doses of the combined agents.
Source : http://www.biospace.com/news_story.aspx?NewsEntityId=118501
Monday, December 7, 2009
To date, researchers have had no success in destroying plaques in the human brain and only minimal success in the laboratory. One reason for these difficulties in finding compounds that can dissolve amyloids is their immense stability and their complex composition.
Yet, Dr. Duennwald ( Boston Biomedical Research Institute , BBRI) and co workers from Pennsylvania School of Medicine, experienced success in previous studies when he exposed amyloids in living yeast cells to EGCG (see the above structure). Furthermore, he and his collaborators also found before that DAPH-12, (see below structure) too, inhibits amyloid production in yeast.
These findings are significant because it is the first time a combination of specific chemicals (EGCG & DAPH-12) has successfully destroyed diverse forms of amyloids at the same time.
Though the detailed mechanism is still to be established, its a good achievement and hope this combinatorial therapy will help those sufferings from Alzheimer's and other degenerative diseases (Huntington's, and Parkinson's) in the days to come.....
Ref : http://www.nature.com/nchembio/journal/v5/n12/pdf/nchembio.246.pdf
Sunday, December 6, 2009
Nizatidine is a histamine H2-receptor antagonist that inhibits stomach acid production, and commonly used in the treatment of peptic ulcer disease (PUD) and gastroesophageal reflux disease (GERD). It was developed by Eli Lilly and is marketed under the trade names Tazac and Axid.
Recently FDA approved the Nizatidine Oral Solution in the 15 mg/mL strength. Nizatidine Oral Solution is the first available generic in oral solution form and marks Amneal’s fourth liquid approval. It represents the company’s first exclusive generic – Amneal has 180-day exclusivity to market the product beginning from the date of first shipment......
Source : http://www.amneal.com/headlines/archive/Nizatidine_Oral_Solution_12-04-09.pdf
Saturday, December 5, 2009
More....First live targeting of tumors with RNA-based technology
Friday, December 4, 2009
Ref : http://www.e-nmr.eu/CASD-NMR
Thursday, December 3, 2009
The researchers (Dr. E. Dale Abel, chief of the endocrinology and metabolism division at the University of Utah School of Medicine in Salt Lake City) found that when insulin-producing beta cells in the pancreas can't respond to circulating insulin, it triggers a "molecular cascade" that damages the normal action of a certain molecular receptor on the surface of the mitochondria. The damaged mitochondria then begin to destroy adenosine triphosphate, the prime fuel for cellular activity. As a result, the beta cells die.
The study provides novel insights into the role of insulin signaling in the regulation of the BAD/GK complex, glycolytic enzyme activity and mitochondrial metabolism in pancreatic β-cells. Ser112-BADS and its upstream kinases may be potential targets for the maintenance of the BAD/GK complex that is necessary for normal mitochondrial function and the regulation of β-cell survival....
Source : http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0007983
Wednesday, December 2, 2009
More....CCII capsules offer safe and effective treatment for rheumatoid arthritis
In its Phase 2 trial of PH-10 for atopic dermatitis (“eczema”), preliminary data from the first 18 subjects indicated that 94% of subjects had improvement in the Eczema Area Severity Index (EASI) during four weeks of treatment. Subjects applied PH-10 daily for up to four weeks to skin areas affected by atopic dermatitis, with response observed weekly throughout this treatment phase and for one month after the end of this period. As in the psoriasis study, the treatments were generally well tolerated with no significant safety issues identified. Hope a sigh of relief for those suffering from psoriasis and atopic dermatitis....
Ref : http://www.pvct.com/pressrelease.html?article=20091201
Tuesday, December 1, 2009
Rivaroxaban is undergoing review by the FDA, On March 19, 2009, an advisory panel recommended FDA approval of rivaroxaban 10 mg once daily for use in patients undergoing hip or knee replacement surgery. The advisory panel concluded that the record trials demonstrate that rivaroxaban is non-inferior and possibly superior to subcutaneous enoxaparin 40 mg once daily. However, they also found an increased risk of bleeding with rivaroxaban and did not address the question of long-term (i.e. > 35 days) use. The advisory panel noted that 1 participant out of 6183 randomized to rivaroxaban died of liver toxicity.....
Monday, November 30, 2009
S-Methylmethionine, or S-methyl-L-methionine, is a derivative of methionine In plants, it is produced from methionine by the enzyme methionine S-methyltransferase. S-Methyl- methionine is sometimes called vitamin U in naturopathic medicine, but it is not recognized as a vitamin by mainstream nutrition science. Methionine in itself has not been demonstrated as effective for treating peptic and duodenal ulcers. Its proponents claim that sources of methionine are limited, or claim it can be found only in raw cabbage; however, these claims are incorrect. Methionine is a common amino acid found in a wide variety of fruits, vegetables, and legumes.
More interesting results by the researchers from the Stanford University, have further substantiated the claim that it can be used to treat peptic and duodenal ulcers.
Acetaminophen is a pain reliever present in many over-the-counter cold and flu medicines. It is broken down, or metabolized, in the body into byproducts , one of which can be very toxic to the liver. At normal, therapeutic levels, this byproduct is easily deactivated when it binds to a naturally occurring, protective molecule called glutathione. But the body's glutathione stores are finite, and are quickly depleted when the recommended doses of acetaminophen are exceeded. Acetaminophen overdose is the most common cause of liver transplantation and the only effective antidote is an unpalatable compound called NAC that can induce nausea and vomiting, and must be administered as soon as possible after the overdose.
As per the claim by the authors, an enzyme called Bhmt2 helped to generate more glutathione. Bhmt2 works by converting the diet-derived molecule S-methylmethionine, or SMM, into methionine, which is subsequently converted in a series of steps into glutathione. The researchers confirmed the importance of the pathway by showing that SMM conferred protection against acetaminophen-induced liver toxicity only in strains of mice in which the Bhmt2 pathway was functional.
By administering SMM, which is found in every flowering plant and vegetable, we were able to prevent a lot of the drug’s toxic effect,” said Peltz. He and his colleagues are now working to set up clinical trials at Stanford to see whether it will have a similar effect in humans. In the meantime, though, he cautions against assuming that dosing oneself with SMM will protect against acetaminophen overdose....
Source : http://med.stanford.edu/ism/2009/november/peltz.html
Sunday, November 29, 2009
The drug brings three copper chaperones into close quarters, weaving them together through an intricate metal-sulfur cluster in a manner that essentially shuts down the copper ferrying system.
The nest-shaped structure of the metal-sulfur cluster discovered by the researchers was completely unanticipated. The sulfur atoms in the tetrathiomolybdate bound to the copper atoms to form an open cluster that bridged the chaperone proteins. In this manner, three copper proteins were jammed onto one thiomolybdate. More interestingly the structure of the complex has been concluded by X-ray studies. Based on the structure and additional experiments, the scientists propose that the drug inhibits the traffic of copper within the cell because of its ability to sequester copper chaperones and their cargo in clusters, rendering the copper inactive.
Ref : http://www.northwestern.edu/newscenter/stories/2009/11/crystal.html
Saturday, November 28, 2009
For decades, it has been known that palmitoylethanolamide (PEA), is a potent anti-inflammatory substance that reduces both allergic symptoms and occurrences of rheumatic fever, but researchers understood little about how PEA works. But now Daniele Piomelli, the Louise Turner Arnold (Chair in Neurosciences at UCI), and colleagues found that levels of PEA are tightly regulated by immune system cells. In turn, PEA helps control the activity of these cells, which are called into action to fight infection, disease and injury in the body. In addition, they found that PEA - also present in foods like eggs and peanuts , is deactivated by a protein called N-acylethanolamine-hydrolyzing acid amidase, which is an enzyme that breaks down molecules controlling cell inflammation.
As most of the antiinflammatory drugs available these days have side effects, this drug may be a boon to the sufferers....
Ref : http://today.uci.edu/news/nr_PEA_091116.php
Details ..........Generating electricity from air flow
As per the claim by the authors, siRNA, works by preventing the gene with the mutation from being expressed but permitting the healthy keratin genes to function normally. The study marked the first time that the skin of a human subject was treated with this type of drug. Researchers say that in this single patient trial the drug worked, had no serious side effects, and has vast potential because of its ability to specifically and potently target single molecules, making it an option for many other genetic diseases, including cancer.
The patient was treated with siRNA on her right foot and with placebo on the left foot. The callus on the right foot that received the siRNA fell off at the site of injection, but this did not happen on the left foot. Congrats for this remarkable achievement...
Source : http://healthcare.utah.edu/dermatology/about/faculty/sancyleachman.html
Friday, November 27, 2009
About Tramadol :
Tramadol is a centrally acting analgesic, used for treating moderate to severe pain. Tramadol was developed by the German pharmaceutical company Grünenthal GmbH in the late 1970.
Tramadol possesses agonist actions at the μ-opioid receptor and affects reuptake at the noradrenergic and serotonergic systems. Tramadol is a compound with mild and delayed μ-agonist activity.
Tramadol is a synthetic stripped-down analog of Codeine and, as such, is an opioid. The opioid agonistic effect of tramadol and its major metabolite(s) almost exclusively effects the μ-opioid receptor. This characteristic is notable, because even morphine is not exclusive to the μ-receptor, although it manifests the preponderance of its opioid agonistic effects here. Tramadol is used to treat moderate to moderately severe pain and most types of neuralgia, including trigeminal neuralgia.
Recently, Par Pharmaceutical Companies, Inc received FDA approval for the abbreviated New Drug Application for the 100mg and 200mg strengths of tramadol ER.....Source : http://www.parpharm.com/media/NR_20091116.jsp
Wednesday, November 25, 2009
Oncolytics Biotech's REOLYSIN combined with paclitaxel and carboplatin well tolerated for advanced cancers
Oncolytics Biotech's REOLYSIN combined with paclitaxel and carboplatin well tolerated for advanced cancers
Nicardipine is a dihydropyridine calcium-channel blocking agent used for the treatment of vascular disorders such as chronic stable angina, hypertension, and Raynaud's phenomenon. It is available in oral and intravenous formulations. Its mechanism of action and clinical effects closely resemble those of nifedipine and the other dihydropyridines (amlodipine, felodipine), except that nicardipine is more selective for cerebral and coronary blood vessels. Furthermore, nicardipine does not intrinsically decrease myocardial contractility and may be useful in the management of congestive heart failure. Nicardipine also has a longer half-life than nifedipine. Nicardipine was approved by the FDA in December 1988. The patent for both Cardene and Cardene SR expired in October 1995.
Recently, Caraco Pharmaceutical Laboratories, Ltd. has launched Nicardipine Hydrochloride Injection immediately following Sun Pharma's final approval from the US Food and Drug Administration (FDA).
Nicardipine Hydrochloride Injection is indicated for the short-term treatment of hypertension when oral therapy is not feasible or not desirable. These Nicardipine Hydrochloride Injections are available as 25 mg/10ml single use ampuls containing 2.5 mg/ml of the drug....
Source : http://phx.corporate-ir.net/phoenix.zhtml?c=98920&p=irol-newsArticle_Print&ID=1356898&highlight=
Tuesday, November 24, 2009
We know that most of the NSAIDs are associated with ulcerogenecity. Though there are many compounds with different mode of action have been tested (and some of them are being used) to treat the peptic ulcer, compounds with phosphodiesterase 5 inhibitor were not tested before Dr. Karakaya of Zonguldak Karaelmas University-who have reported that Vardenafil can be used to treat the NSAID-induced gastric ulcer. As per the claim by the researchers the activity is dose dependent.
Ref : http://www.wjgnet.com/1007-9327/abstract_en.asp?f=5091&v=15
Monday, November 23, 2009
The researchers subjected spinal cord tissue to stresses that mimic what happens in a compression injury, which stretches nerves. Then they treated the damaged axons with 4-aminopyridine-3-methyl hydroxide. The same drug is used primarily as a research tool and also to manage symptoms of multiple sclerosis.
The axons of each nerve are sheathed in a thick insulating lipid layer, called myelin, which enables the transmission of signals without short circuiting, much like the insulation surrounding electrical wires. Spinal cord trauma damages the myelin sheath, exposing "fast potassium channels" that are embedded in the axons and are critical for transmitting nerve impulses.
The researchers also discovered that 4-aminopyridine-3-methyl hydroxide is a "potassium channel blocker," using a sophistic laboratory technique called "patch clamp" to measure signal conduction. Findings confirmed that the compound prevents the exposed channels from leaking electrical current and enhances nerve conduction in segments of the damaged spinal cord. The compound could make it possible to sidestep spinal cord damage by enabling axons to transmit signals as though they were still sheathed in myelin.
As per the claim by the researchers, the new compound is about 10 times more potent than 4-aminopyridine, meaning lower doses can be used to reduce the likelihood of serious side effects. Because myelin also is damaged in multiple sclerosis, the same drug might be used to restore nerve function in people stricken with the disease. Hope in the days to come patients suffering from Multiple sclerosis and spinal cord injuries will breathe a sigh of relief...
Ref : J Neurophysiol (November 18, 2009). doi:10.1152/jn.00154.2009.
Sunday, November 22, 2009
Now researchers from the University of Pennsylvania, have found an interesting fact that the antioxidant thiocyanate normally existing in the body protects lung cells from injuries caused by accumulations of hydrogen peroxide and hypochlorite, the active ingredient in household bleach. These potentially harmful chemicals are made by the body as a reaction to infection and injury. In addition, thiocyanate also protects cells from hypochlorite produced in reactions involving MPO, an enzyme released from germ-fighting white blood cells during inflammation.
The research team demonstrated that in three additional cell types used to extend their ideas to other inflammation-related conditions - cardiovascular disease, neurodegeneration, and diabetes - thiocyanate at blood concentrations of at least 100 micromolar (micromoles per liter) greatly reduces the toxicity of MPO in cells, including those lining blood vessels. Humans naturally derive thiocyanate from some vegetables and blood levels of thiocyanate in the general population vary from 10 to 140 micromolar.
So without an adequate dietary supply of thiocyanate (from broccoli & Cauliflower), hypochlorite produced by the body during inflammation would cause additional collateral damage to cells, thus worsening inflammatory diseases, and predisposing humans to diseases linked to MPO activity, including atherosclerosis. Thus the authors claim that delivering thiocyanate directly to the digestive and respiratory systems might be a therapy for CF disease.