Adverse Event Reporting System (AERS)

The Adverse Event Reporting System (AERS) is a computerized information database designed to support the FDA's post-marketing safety surveillance program for all approved drug and therapeutic biologic products. The FDA uses AERS to monitor for new adverse events and medication errors that might occur with these marketed products.

Reporting of adverse events from the point of care is voluntary in the United States. FDA receives some adverse event and medication error reports directly from health care professionals (such as physicians, pharmacists, nurses and others) and consumers (such as patients, family members, lawyers and others). Healthcare professionals and consumers may also report these events to the products’ manufacturers. If a manufacturer receives an adverse event report, it is required to send the report to FDA as specified by regulations. The MedWatch site provides information about mandatory reporting.

The structure of AERS is in compliance with the international safety reporting guidance (ICH E2B ) issued by the International Conference on Harmonisation. Adverse events in AERS are coded to terms in the Medical Dictionary for Regulatory Activities terminology (MedDRA).

AERS is a useful tool for FDA, which uses it for activities such as looking for new safety concerns that might be related to a marketed product, evaluating a manufacturer's compliance to reporting regulations and responding to outside requests for information. The reports in AERS are evaluated by clinical reviewers in the Center for Drug Evaluation and Research (CDER) and the Center for Biologics Evaluation and Research (CBER) to monitor the safety of products after they are approved by FDA. If a potential safety concern is identified in AERS, further evaluation might include epidemiological studies. Based on an evaluation of the potential safety concern, FDA may take regulatory action(s) to improve product safety and protect the public health, such as updating a product’s labeling information, restricting the use of the drug, communicating new safety information to the public, or, in rare cases, removing a product from the market.

AERS data do have limitations. First, there is no certainty that the reported event was actually due to the product. FDA does not require that a causal relationship between a product and event be proven, and reports do not always contain enough detail to properly evaluate an event. Further, FDA does not receive all adverse event reports that occur with a product. Many factors can influence whether or not an event will be reported, such as the time a product has been marketed and publicity about an event. Therefore, AERS cannot be used to calculate the incidence of an adverse event in the U.S. population.

• AERS Data
• AERS Data Files
• AERS Statistics

How to Report Adverse Events

• MedWatch: The FDA Safety Information and Adverse Event Reporting Program
• Voluntary Reporting to FDA

1. Reporting by Consumers
2. Reporting by Health Professionals

• Mandatory Reporting by Drug/Biologics Manufacturers, Distributors, and Packers

FDA to Communicate Safety Monitoring Activities to Consumers and Health Care Professionals

The U.S. Food and Drug Administration unveiled a new source of information for patients and health care professionals on the safety of recently approved drugs and biologics.
Summaries of FDA safety analyses on recently approved products will now be periodically prepared and posted on FDA's website along with a brief discussion of the steps FDA is taking to address any identified safety issues.

Some side effects may not become apparent until after a medicine has been approved and becomes available to a larger, more diverse population than the patients who participated in clinical trials that supported approval. The new summaries provide a comprehensive look at safety data early in the product's post-approval life cycle and are based on reports by manufacturers, providers, consumers and others to the FDA's Adverse Event Reporting System (AERS) and the Vaccine Adverse Event Reporting System maintained by the FDA and the Center for Disease Control and Prevention; periodic safety information submitted to FDA by manufacturers; information contained in the medical literature; and data from ongoing drug and biologic studies.

Included in the summaries may be information on potentially serious, previously unidentified risks, if any are found during the review, as well as known adverse events that occur more often than they did during clinical studies. The summaries will also include a brief discussion of any steps FDA may be taking to address these safety issues.

Under Section 915 of the Food and Drug Administration Amendments Act of 2007 (FDAAA), FDA is required to prepare the safety summaries within 18 months after a product's approval or after it has been used by 10,000 patients, whichever comes later.

"Conducting systematic, comprehensive, safety reviews of recently approved drugs and biologics provides an early detection mechanism for potentially serious risks and complements the FDA's analysis of safety data during drug development and the agency's routine monitoring of safety information after product approval," said Gerald Dal Pan, M.D., M.H.S., director of the Office of Surveillance and Epidemiology in the FDA's Center for Drug Evaluation and Research.

"These summaries will provide clear and useful information in a timely manner that can be used by providers and patients to make informed decisions about an individual's health," said Robert Ball, M.D., M.P.H., Sc.M., director of the Office of Biostatistics and Epidemiology in the Center for Biologics Evaluation and Research.

Initial summary reports will contain information on drugs and biologics approved since September 2007, including several drugs for infections, hypertension, depression and other conditions. The summary reports will be located on an FDA Web page that was first established in 2008 to serve as a portal for drug safety information.

How to Add Search form to Blogger

If you are new to Blogger then you should know that there are lots of chances that Search form get missing from your blogger homepage, if you want to add search form in your blogger homepage then I will help you to do so. For adding search form at homepage you have to follow the instructions given below:

1. Sign In to your Blogger Account.
2. Under Template >Page Elements tab.
3. Click “Add a Page Element”.
4. Select HTML/JavaScript and add the below codes:

Form Style 1

Code:

<span style="color: rgb(102, 0, 204);">readonly</span>="readonly"><form id="”searchThis”" action="”/search”" style="”display:inline;”" method="”get”"><input id="”searchBox”" name="”q”" type="”text”/"> <input id="”searchButton”" value="”Go”" type="”submit”/"></form><br />

Form Style 2

Code:

<span style="color: rgb(102, 0, 204);">readonly</span>="readonly"><br /><form id="”searchthis”" action="”/search”" style="”display:inline;”" method="”get”"><br /><input id="”search-box”" name="”q”" size="”25″" type="”text”" style="”background:"> <input id="”search-btn”" value="”Search”" type="”submit”" style="”background:"></form><br />

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Prasugrel

Prasugrel (marketing name Effient in the US, Efient in EU and Prasita in India) is a novel platelet inhibitor developed by Daiichi Sankyo Co. and produced by Ube and currently marketed in the United States in cooperation with Eli Lilly and Company for acute coronary syndromes planned for percutaneous coronary intervention (PCI). Prasugrel was approved for use in Europe in February 2009, and is currently available in the UK. On July 10, 2009, the US Food and Drug Administration approved the use of prasugrel for the reduction of thrombotic cardiovascular events (including stent thrombosis) in patients with acute coronary syndrome who are to be managed with PCI.
Pharmacology:

Prasugrel is a member of the thienopyridine class of ADP receptor inhibitors, like ticlopidine (trade name Ticlid) and clopidogrel (trade name Plavix). These agents reduce the aggregation ("clumping") of platelets by irreversibly binding to P2Y₁₂ receptors. Compared to clopidogrel, "prasugrel(trade name apagrel) inhibits adenosine diphosphate–induced platelet aggregation more rapidly, more consistently, and to a greater extent than do standard and higher doses of clopidogrel in healthy volunteers and in patients with coronary artery disease, including those undergoing PCI". Unlike clopidogrel, which was issued a black box warning from the FDA on March 12, 2010, .prasugrel has not been shown to carry those same limitations.

Pharmacodynamics

Prasugrel produces inhibition of platelet aggregation to 20 μM or 5 μM ADP, as measured by light transmission aggregometry. Following a 60-mg loading dose of Effient, approximately 90% of patients had at least 50% inhibition of platelet aggregation by 1 hour. Maximum platelet inhibition was about 80% (Figure 2). Mean steady-state inhibition of platelet aggregation was about 70% following 3 to 5 days of dosing at 10 mg daily after a 60-mg loading dose of Effient. Platelet aggregation gradually returns to baseline values over 5-9 days after discontinuation of prasugrel, this time course being a reflection of new platelet production rather than pharmacokinetics of prasugrel. Discontinuing clopidogrel 75 mg and initiating prasugrel 10 mg with the next dose resulted in increased inhibition of platelet aggregation, but not greater than that typically produced by a 10 mg maintenance dose of prasugrel alone. The relationship between inhibition of platelet aggregation and clinical activity has not been established.

Pharmacokinetics:

Prasugrel is a prodrug and is rapidly metabolized to a pharmacologically active metabolite and inactive metabolites. The active metabolite has an elimination half-life of about 7 hours (range 2-15 hours). Healthy subjects, patients with stable atherosclerosis, and patients undergoing PCI show similar pharmacokinetics.

ABSORPTION AND BINDING - Following an oral administration, ≥ 79% of the dose is absorbed. The absorption and metabolism are rapid, with peak plasma concentrations (C_max) of the active metabolite occurring approximately 30 minutes after dosing. The active metabolite’s exposure (AUC) increases slightly more than proportionally over the dose range of 5 to 60 mg. Repeated daily doses of 10 mg do not lead to accumulation of the active metabolite. In a study of healthy subjects given a single 15 mg dose, the AUC of the active metabolite was unaffected by a high fat, high calorie meal, but C_max was decreased by 49% and T_max was increased from 0.5 to 1.5 hours. Effient can be administered without regard to food. The active metabolite is bound about 98% to human serum albumin.

METABOLISM AND ELIMINATION - Prasugrel is not detected in plasma after oral administration. It is rapidly hydrolyzed in the intestine to a thialactone, which is then converted to the active metabolite by a single step, primarily by the CYP3A4 and CYP2B6 and to a lesser extent by the CYP2C9 and CYP2C19. The estimates of apparent volume of distribution of prasugrel's active metabloite range from 44 to 68 L and the estimates of apparent clearance range from 112 to 166 L/hr in healthy subjects and patients with stable atherosclerosis. The active metabolite is metabolized to two inactive compounds by S-methylation or conjugation with cysteine. The major inactive metabolites are highly bound to human plasma proteins. Approximately 68% of the prasugrel dose is excreted in the urine and 27% in the feces as inactive metabolite.

DRUG INTERACTIONS

Potential for Other Drugs to Affect Prasugrel

Inhibitors of CYP3A - Ketoconazole (400 mg daily), a selective and potent inhibitor of CYP3A4 and CYP3A5, did not affect prasugrel-mediated inhibition of platelet aggregation or the active metabolite’s AUC and Tmax, but decreased the Cmax by 34% to 46%. Therefore, CYP3A inhibitors such as verapamil, diltiazem, indinavir, ciprofloxacin, clarithromycin, and grapefruit juice are not expected to have a significant effect on the pharmacokinetics of the active metabolite of prasugrel.

Inducers of Cytochromes P450 - Rifampicin (600 mg daily), a potent inducer of CYP3A and CYP2B6 and an inducer of CYP2C9, CYP2C19, and CYP2C8, did not significantly change the pharmacokinetics of prasugrel’s active metabolite or its inhibition of platelet aggregation. Therefore, known CYP3A inducers such as rifampicin, carbamazepine, and other inducers of cytochromes P450 are not expected to have significant effect on the pharmacokinetics of the active metabolite of prasugrel.

Drugs that Elevate Gastric pH - Daily coadministration of ranitidine (an H2 blocker) or lansoprazole (a proton pump inhibitor) decreased the Cmax of the prasugrel active metabolite by 14% and 29%, respectively, but did not change the active metabolite’s AUC and Tmax. In TRITON-TIMI 38, Effient was administered without regard to coadministration of a proton pump inhibitor or H2 blocker.

Statins - Atorvastatin (80 mg daily), a drug metabolized by CYP450 3A4, did not alter the pharmacokinetics of prasugrel’s active metabolite or its inhibition of platelet aggregation.

Heparin - A single intravenous dose of unfractionated heparin (100 U/kg) did not significantly alter coagulation or the prasugrel-mediated inhibition of platelet aggregation; however, bleeding time was increased compared with either drug alone.

Aspirin - Aspirin 150 mg daily did not alter prasugrel-mediated inhibition of platelet aggregation; however, bleeding time was increased compared with either drug alone.

Warfarin - A significant prolongation of the bleeding time was observed when prasugrel was coadministered with 15 mg of warfarin.

Potential for Prasugrel to Affect Other Drugs

In vitro metabolism studies demonstrate that prasugrel’s main circulating metabolites are not likely to cause clinically significant inhibition of CYP1A2, CYP2C9, CYP2C19, CYP2D6, or CYP3A, or induction of CYP1A2 or CYP3A.

Drugs Metabolized by CYP2B6 — Prasugrel is a weak inhibitor of CYP2B6. In healthy subjects, prasugrel decreased exposure to hydroxybupropion, a CYP2B6-mediated metabolite of bupropion, by 23%, an amount not considered clinical significant. Prasugrel is not anticipated to have significant effect on the pharmacokinetics of drugs that are primarily metabolized by CYP2B6, such as halothane, cyclophosphamide, propofol, and nevirapine.

Effect on Digoxin - The potential role of prasugrel as a Pgp substrate was not evaluated. Prasugrel is not an inhibitor of Pgp, as digoxin clearance was not affected by prasugrel coadministration.

Pharmacogenomics

There is no relevant effect of genetic variation in CYP2B6, CYP2C9, CYP2C19, or CYP3A5 on the pharmacokinetics of prasugrel’s active metabolite or its inhibition of platelet aggregation.
TRITON-TIMI 38 study

As published in the New England Journal of Medicine's online edition, the TRITON-TIMI 38 study of 13,608 patients with acute coronary syndromes compared prasugrel against clopidogrel, both in combination with aspirin, and found that, as a more potent anti-platelet agent, prasugrel reduced the combined rate of death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke (12.1% for clopidogrel vs. 9.9% for prasugrel). This difference in the primary endpoint was mainly driven by the reduction of non-fatal myocardial infarctions. However, an increased rate of serious bleedings (1.4%, vs. 0.9% in the clopidogrel group) and fatal bleedings (0.4% vs. 0.1%) was also observed. Overall mortality did not differ between the two treatment groups.

From the editorial in the NEJM, "In TRITON–TIMI 38, for each death from cardiovascular causes prevented by the use of prasugrel as compared with clopidogrel, approximately one additional episode of fatal bleeding was caused by prasugrel".

In patients with acute coronary syndromes (ACS) undergoing percutaneous coronary intervention (PCI), prasugrel was associated with a significantly lower incidence of ischemic events than clopidogrel, and was particularly effective in specific subgroups of patients, such as those with diabetes mellitus. In this sub-group there is a 30% relative risk reduction (4.2% ARR for unstable angina/NSTEMI and 5% AAR for STEMI) compared to the clopidogrel group without significant increased risk for major bleeding(2.2% vs. 2.3%). However, the efficacy of prasugrel was offset by a higher risk of bleeding than clopidogrel, with patients aged ≥75 years, those weighing <60>

Ranbaxy Launches Antiplatelet Agent Prasugrel in India

Daiichi Sankyo Company Limited ("Daiichi Sankyo") and Ranbaxy Laboratories Limited ("Ranbaxy") announced today that Ranbaxy has launched a generic version of prasugrel in India. The product, called Prasita, is an antiplatelet agent for the prevention of atherothrombotic events in patients with acute coronary syndrome undergoing percutaneous coronary intervention. Prasita is solely marketed by Ranbaxy in India.

Following the April 2009 launch of Olvance (olmesartan medoxomil), an antihypertensive originally discovered by Daiichi Sankyo, Prasita is the second product from the Daiichi Sankyo portfolio to be introduced in India through the strong Ranbaxy business network. Ranbaxy will create awareness, understanding and acceptance of the new antiplatelet therapy among the target audiences in the country.

"We are pleased to be able to introduce Prasita in India," said Atul Sobti, CEO and Managing Director of Ranbaxy. "A number of synergy projects between Ranbaxy and Daiichi Sankyo are already underway, and we will further strengthen our common endeavour to realize greater benefits from our Hybrid Business Model."

"The launch of our two top flagship products, olmesartan medoxomil and prasugrel, by Ranbaxy shows our serious commitment to India, and we will continue to explore further collaborations leveraging the Hybrid Business Model," said Takashi Shoda, President & CEO of Daiichi Sankyo.

About Daiichi Sankyo
The Daiichi Sankyo Group is dedicated to the creation and supply of innovative pharmaceutical products to address the diversified, unmet medical needs of patients in both mature and emerging markets. While maintaining its portfolio of marketed pharmaceuticals for hypertension, hyperlipidemia, and bacterial infections, the Group is engaged in the development of treatments for thrombotic disorders and focused on the discovery of novel oncology and cardiovascular-metabolic therapies. Furthermore, the Daiichi Sankyo Group has created a "Hybrid Business Model," which will respond to market and customer diversity and optimize growth opportunities across the value chain. For more information, please visit www.daiichisankyo.com.

About Ranbaxy Laboratories Limited
Ranbaxy Laboratories Limited, India's largest pharmaceutical company, is an integrated, research based, international pharmaceutical company producing a wide range of quality, affordable generic medicines, trusted by healthcare professionals and patients across geographies. Ranbaxy’s continued focus on R&D has resulted in several approvals in developed markets and significant progress in New Drug Discovery Research. The Company’s foray into Novel Drug Delivery Systems has led to proprietary "platform technologies," resulting in a number of products under development. The Company is serving its customers in over 125 countries and has an expanding international portfolio of affiliates, joint ventures and alliances, ground operations in 46 countries and manufacturing operations in 7 countries. Ranbaxy is a member of the Daiichi Sankyo Group. Daiichi Sankyo is a leading global pharma innovator, headquartered in Tokyo, Japan.

Anti frustation software! Soluto

Enjoy your PC

Frustrated by your sluggish and unresponsive PC?

Soluto is bringing an end to PC user frustration with transparency, killer technology, and your help

Try Soluto, the “Anti-Frustration Software“…

I consider myself a techie, but I must admit I’ve more than once struggled to find out what is causing my computer to slow down to slooooooooooooooow motion at times. So when I discovered Soluto I was more than willing to give it a go. I can hear you – Pffft, yet another enhancement software. Well sort of, or…

New apporach

Soluto is a new way of thinking. The software is connected to an online community which will store your frustrating moments and offer solutions based on what others have done on their system. Don’t think it’s just another community thing, because Soluto also includes scanning technology that monitors your running applications and which drivers and resources they use. All you have to do is press the “I’m frustrated Button” and you activate the solution centre. Based on user’s experiences you can get feedback on what should work for you and what will definitively not.

What really makes Soluto stand out is that you can use it no matter your technical expertise. The solution is People Oriented, not vise versa.

Speeding up…

After I installed it Soluto asked me to reboot so it could measure how long time it took to reboot. After the reboot Soluto then searched through its community checking all the software and system drivers launched at boot time. Then came back with suggestions to which could be entirely could be removed or set to launch after boot up.

Boot took initially 2 minutes and 44 seconds. After some suggested tweaking through the Soluto interface I reduced boot up time with 55 seconds. Not bad for a start.

Upcoming

At the moment Soluto is based on your feedback or action. The developers behind Soluto is also working on an automated (anonymous) feature which I’m told is going to collect, analyze and share its find with developers. Much the same as we at mintywhite let you tell developers what you think about their software. “By sheer exposure of this information, Soluto will help software vendors to start prioritizing the user by designing products with a smooth, frustration-free user experience in mind.”

Soluto - How to use Soluto Beta from Soluto on Vimeo.

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