Friday, 28 February 2014

Sciatica pain

Sciatica is a common type of pain affecting the sciatic nerve, a large nerve extending from the lower back down the back of each leg.

What Are the Symptoms of Sciatica?

Common symptoms of sciatica include:
  • Pain in the rear or leg that is worse when sitting
  • Burning or tingling down the leg
  • Weakness, numbness, or difficulty moving the leg or foot
  • A constant pain on one side of the rear
  • A shooting pain that makes it difficult to stand up
Sciatica usually affects only one side of the lower body. Often, the pain extends from the lower back all the way through the back of the thigh and down through the leg. Depending on where the sciatic nerve is affected, the pain may also extend to the foot or toes.
For some people, the pain from sciatica can be severe and debilitating. For others, the sciatica pain might be infrequent and irritating, but has the potential to get worse.
Seek immediate medical attention with any symptoms of progressive lower extremity weakness and/or loss of bladder or bowel control.

What Causes Sciatica?

Sciatica is caused by irritation of the root(s) of the lower lumbar and lumbosacral spine.
Additional common causes of sciatica include:
  • Lumbar spinal stenosis (narrowing of the spinal canal in the lower back)
  • Degenerative disc disease (breakdown of discs, which act as cushions between the vertebrae)
  • Spondylolisthesis (a condition in which one vertebra slips forward over another one)
  • Pregnancy
Other things that may make your back pain worse include being overweight, not exercising regularly, wearing high heels, or sleeping on a mattress that is too soft.

Friday, 21 February 2014

Pharma blog: ELISA (Enzyme-Linked ImmunoSorbant Assay): Trouble...

Pharma blog: ELISA (Enzyme-Linked ImmunoSorbant Assay): Trouble...: 1. Positive results in negative control Contamination of reagents/samples May be contamination of reagents or samples, or cross ...

ELISA (Enzyme-Linked ImmunoSorbant Assay): Troubleshoout Problem solving tips

1. Positive results in negative control

Contamination of reagents/samples
May be contamination of reagents or samples, or cross contamination from splashing between wells. Use fresh reagents and pipette carefully.
Sandwich ELISA – detection antibody is detecting coating antibody
Check the correct coating antibody and detection antibodies are being used and that they will not detect each other.
Insufficient washing of plates
Ensure well areas are washed adequately by filling the wells with wash buffer. Ensure all residual antibody solutions are removed before washing.
Too much antibody used leading to non-specific binding
Check the recommended amount of antibody suggested. Try using less antibody.

2. High background across entire plate

Conjugate to strong or left on too long
Check dilution of conjugate, use it at the recommended dilution. Stop the reaction using stop buffer as soon as the plate has developed enough for absorbance readings.
Substrate solution or stop solution is not fresh
Use fresh substrate solution. Stop solution should be clear (if it has gone yellow, this is a sign of contamination and it should be replaced).
Reaction not stopped
Color will keep developing if the substrate reaction is not stopped.
Plate left too long before reading on the plate reader
Color will keep developing (though at a slower rate if stop solution has been added).
Contaminants from laboratory glassware
Ensure reagents are fresh and prepared in clean glassware. Sterilize glassware beforehand if possible.
Substrate incubation carried out in the light
Substrate incubation should be carried out in the dark.
Incubation temperature too high
Antibodies will have optimum binding activity at the correct temperature. Ensure the incubations are carried out at the correct temperature and that incubators are set at the correct temperature and working. Incubation temperature may require some optimization.
Non-specific binding of antibody
Ensure a block step is included and a suitable blocking buffer is being used. We recommend using 5-10 % serum from the same species of the secondary antibody, or bovine serum.
Ensure wells are pre-processed to prevent non specific attachment. Use an affinity purified antibody, preferably pre-absorbed.
Also check suggestions listed under ‘Positive results in negative control’

3. Low absorbance values

Target protein not expressed in sample used/ Low level of target protein expression in sample used
Check the expression profile of the target protein to ensure it will be expressed in your samples. If there is low level of target protein expression, increase the amount of sample used, or you may need to change to a more sensitive assay. Ensure you are using a positive control within the detection range of the assay.
Insufficient antibody
Check the recommended amount of antibody is being used. The concentration of antibody may require increasing for optimization of results.
Substrate solutions not fresh or combined incorrectly
Prepare the substrate solutions immediately before use. Ensure the stock solutions are in date and have been stored correctly, and are being used at the correct concentration. Ensure the reagents are used as directed at the correct concentration.
Reagents not fresh or not at the correct pH
Ensure reagents have been prepared correctly and are in date.
Incubation time not long enough
Ensure you are incubating the antibody for the recommended amount of time, if an incubation time is suggested. The incubation time may require increasing for optimization of results.
Incubation temperature too low
Antibodies will have optimum binding activity at the correct temperature. Ensure the incubations are carried out at the correct temperature and that incubators are set at the correct temperature and working. Incubation temperature may require some optimization. Ensure all reagents are at room temperature before proceeding.
Stop solution not added
Addition of stop solution increases the intensity of color reaction and stabilizes the final color reaction.

4. High absorbance values for samples and/or positive control (absorbance does not go down as the sample is diluted down the plate)

The concentration of samples or positive control is too high and out of range for the sensitivity of the assay. Re-assess the assay you are using OR reduce the concentration of samples and control by dilution before adding to the plate. Take the dilution into account when calculating the resulting concentrations.

5. Inconsistent absorbances across the plate

Plates stacked during incubations
Stacking of plates does not allow even distribution of temperature across the wells of the plates. Avoid stacking.
Pipetting inconsistent
Ensure pipettes are working correctly and are calibrated. Ensure pipette tips are pushed on far enough to create a good seal. Take particular care when diluting down the plate and watch to make sure the pipette tips are all picking up and releasing the correct amount of liquid. This will greatly affect consistency of results between duplicates.
Antibody dilutions/reagents not well mixed
To ensure a consistent concentration across all wells, ensure all reagents and samples are mixed before pipetting onto the plate.
Wells allowed to dry out
Ensure lids are left on the plates at all times when incubating. Place a humidifying water tray (bottled clean/sterile water) in the bottom of the incubator.
Inadequate washing
This will lead to some wells not being washed as well as others, leaving different amounts of unbound antibody behind which will give inconsistent results.
Bottom of the plate is dirty affecting absorbance readings
Clean the bottom of the plate carefully before re-reading the plate.

6. Color developing slowly

Plates are not at the correct temperature
Ensure plates are at room temperature and that the reagents are at room temperature before use.
Conjugate too weak
Prepare the substrate solutions immediately before use. Ensure the stock solutions are in date and have been stored correctly, and are being used at the correct concentration. Ensure the reagents are used as directed, at the correct concentration.
Contamination of solutions
Presence of contaminants, such as sodium azide and peroxidase can affect the substrate reaction. Avoid using reagents containing these preservatives.

Monday, 17 February 2014

Pharma blog: angiotensin receptor : An overview

Pharma blog: angiotensin receptor : An overview: Plasma-membrane receptors for angiotensin II (AII) have been identified in many AII-responsive tissues involved in the control of blood...

angiotensin receptor : An overview

Plasma-membrane receptors for angiotensin II (AII) have been identified in many AII-responsive tissues involved in the control of blood pressure via direct or indirect actions on vascular contractility. The specific, high-affinity receptors for AII in adrenal zona glomerulosa, vascular smooth muscle, kidney, brain, and anterior pituitary gland exhibit generally similar binding properties. However, the AII receptors in adrenal zona glomerulosa and vascular smooth muscle undergo reciprocal regulatory changes during alterations in sodium intake. These appear to be mediated by changes in circulating AII and are accompanied by parallel changes in sensitivity to AII. The AII receptors in the anterior pituitary gland are located in lactotrophs and corticotrophs and mediate the stimulatory actions of AII upon prolactin and ACTH secretion, acting in conjunction with other hypothalamic regulators. The anterior pituitary receptors are not affected by changes in sodium balance or AII infusion, in contrast to adrenal and vascular AII receptors, but exhibit similar ligand-binding properties to the sites present in other tissues. In the brain, AII receptors are present in several discrete regions and are particularly concentrated in the circumventricular organs. During dehydration, AII receptors are increased in the subfornical organ, but show no significant changes in the other circumventricular organs. The increase in subfornical-organ receptors is analogous to the up-regulation of AII sites in the adrenal cortex during sodium deficiency and may have a potentiating action upon the dipsogenic role of AII during dehydration. Mapping of AII receptors of the brain by topical autoradiography has revealed a highly characteristic pattern of distribution in brain regions concerned with drinking, adrenergic control, blood-pressure regulation, and hypothalamic control of pituitary-hormone secretion. In the rat kidney, AII receptors have been localized in the cortex and medulla by topical autoradiography with 125I-[Sar1]AII. The renal cortical receptors appear to be localized in glomeruli, whereas the AII receptors in the renal medulla are distributed diffusely in medullary tissue and also as localized radiating stripes which correspond to the vasa rectae bundles. The location of the renal receptors for AII in cortical and medullary sites emphasizes the multiplicity of actions of the octapeptide upon the individual compartments of the kidney.

The cardiovascular and other actions of angiotensin II (Ang II) are mediated by AT1 and AT2 receptors, which are seven transmembrane glycoproteins with 30% sequence similarity. Most species express a single autosomal AT1 gene, but two related AT1A and AT1B receptor genes are expressed in rodents. AT1 receptors are predominantly coupled to Gq/11, and signal through phospholipases A, C, D, inositol phosphates, calcium channels, and a variety of serine/threonine and tyrosine kinases. Many AT1-induced growth responses are mediated by transactivation of growth factor receptors. The receptor binding sites for agonist and nonpeptide antagonist ligands have been defined. The latter compounds are as effective as angiotensin converting enzyme inhibitors in cardiovascular diseases but are better tolerated. The AT2receptor is expressed at high density during fetal development. It is much less abundant in adult tissues and is up-regulated in pathological conditions. Its signaling pathways include serine and tyrosine phosphatases, phospholipase A2, nitric oxide, and cyclic guanosine monophosphate. The AT2 receptor counteracts several of the growth responses initiated by the AT1 and growth factor receptors. The AT4 receptor specifically binds Ang IV (Ang 3–8), and is located in brain and kidney. Its signaling mechanisms are unknown, but it influences local blood flow and is associated with cognitive processes and sensory and motor functions. Although AT1 receptors mediate most of the known actions of Ang II, the AT2 receptor contributes to the regulation of blood pressure and renal function. The development of specific nonpeptide receptor antagonists has led to major advances in the physiology, pharmacology, and therapy of the renin-angiotensin system.

Thursday, 6 February 2014

Pharma blog: Study of Drug for Blood Clots Caused a Stir, Recor...

Pharma blog: Study of Drug for Blood Clots Caused a Stir, Recor...: The makers of the blood-thinning drug Pradaxa were so worried that an internal research paper would damage drug sales that some employee...

Study of Drug for Blood Clots Caused a Stir, Records Show

The makers of the blood-thinning drug Pradaxa were so worried that an internal research paper would damage drug sales that some employees not only pressured the author to revise it, but suggested it should be quashed altogether, according to newly unsealed legal documents.
The documents were made public last week by a federal judge in Illinois who is overseeing thousands of lawsuits filed by patients and their families, who say that Pradaxa’s manufacturer, the German company Boehringer Ingelheim, failed to properly warn them about the risks of taking the drug.
Since its approval in 2010, the drug, which can cause fatal bleeding, has brought in more than $2 billion in sales in the United States, according to the research firm IMS Health.
It has been prescribed to 850,000 patients, but has also been linked to more than 1,000 deaths.
Boehringer Ingelheim has stood by the drug, noting that the Food and Drug Administration has upheld its safety and that its value has been proved in clinical trials.
Launch media viewer
Documents show that some of Pradaxa’s employees openly fretted about the marketing implications of the study.
Many of the documents released by Chief Judge David R. Herndon of the United States District Court in East St. Louis, which included emails, memos and internal presentations, centered on whether a coming research paper would undercut one of Pradaxa’s main selling points: that it does not require regular blood tests to ensure it is working.
The issue has been hotly debated among heart and stroke specialists, in part because not all people — especially older patients — metabolize the drug the same way, and because there are fewer dose options as well as no tests available for Pradaxa in the United States to monitor those who might be most at risk. An additional dose and a test are available in Europe.
Testing is a critical issue because Pradaxa and two other recently approved drugs, Xarelto and Eliquis, are in a race to gain market share from warfarin, a generic drug that for decades has been the standard treatment for preventing blood clots and strokes. 

Many patients viewed the older warfarin as a nuisance because it requires frequent blood tests and careful attention to diet and other drugs.
The new drugs do not require such monitoring, yet claim to be as good, or better, at preventing strokes and blood clots in patients with a heart-rhythm disorder known as atrial fibrillation.
The documents show that Boehringer Ingelheim employees openly fretted when it appeared that the results of the research paper, written by Paul A. Reilly, a clinical program director at the company, indicated that some patients could benefit from monitoring of their blood. A certain segment of patients, the paper found, absorb too little of the drug to effectively prevent strokes, while another group absorbs so much that they are at a higher risk for bleeding.
In a draft version of the paper included in the court records, Dr. Reilly and his co-authors detailed specific levels of how much Pradaxa should be in a patient’s bloodstream, and said that keeping some patients within that range would help prevent strokes and bleeding.
As Dr. Reilly’s draft paper circulated within the company, some employees questioned what the marketing implications of such a conclusion would be.
One company supervisor, Dr. Jutta Heinrich-Nols, wrote in an email to other employees that she could not believe the company was planning to publish research that would negate a decade’s worth of work proving that patients taking Pradaxa would not need regular tests.
Publishing the research results, she warned, could make it “extremely difficult” for the company to defend its long-held position to regulators that Pradaxa did not require testing.
And, Dr. Heinrich-Nols added in the email, the research, if known, would “undermine” the company’s efforts to compete with other new anticoagulants, such as Xarelto and Eliquis.
“I would like to ask you to check again whether this is really wanted,” she wrote about publishing the research.
Another company leader, Dr. Andreas Clemens, questioned whether legal repercussions would arise if Dr. Reilly’s paper detailed a specific range where the drug worked best. “Maybe I am phobic, but I am not happy with the conclusion,” he wrote.
Still, some of the same employees acknowledged that Dr. Reilly’s paper addressed serious concerns that doctors were raising outside the company. “The world is crying for this information — but the tricky part is that we have to tailor the messages smart,” Dr. Clemens wrote in a separate email.
In emails, Dr. Reilly defended his conclusions, saying the research showed that a minority of patients might benefit from blood testing. “I think we just need to make the message clear,” he said. Dr. Reilly declined to comment, referring questions to the company’s public relations department.
The documents highlight how much information about drug safety is in the hands of people with a financial interest in the outcome, some drug industry observers said.
“With these drugs, this is a really tough call,” said Dr. Lisa M. Schwartz, a professor of medicine at the Dartmouth Institute for Health Policy and Clinical Practice.
“In these situations, where the stakes are really high, how crazy is it that it’s in the hands of people who are so conflicted?” she asked.
Dr. Reilly’s paper was published Tuesday in the Journal of the American College of Cardiology, and although many of the conclusions in the draft version remained, references to a patient’s optimal blood-level range no longer appear in the article.
In a statement, representatives for Boehringer Ingelheim said the recently unsealed documents “represent small fragments of the robust discussion and debate that is a vital component in all scientific inquiry, and in the research and development of any important medication such as Pradaxa.” The company said the changes to the manuscript were made as the scientists’ thinking evolved, and they ultimately concluded that no single blood-level range is ideal for all patients.
Lawyers for the plaintiffs declined to comment.
Pradaxa is approved in a 150-milligram dose, as well as a lower 75-milligram dose for patients with low kidney function. But unlike European regulators, the F.D.A. did not approve a 110-milligram dose because the agency felt the lower dose would not benefit most patients.
Boehringer Ingelheim continued to pursue the approval of the 110-milligram dose even after the higher dose was approved, but the company said it abandoned the effort after concluding that a proposed study and other analyses were not feasible.
Some doctors applauded Boehringer Ingelheim for finally addressing an area of intense interest among cardiologists. Dr. Hugo ten Cate, a professor of medicine at Maastricht University Medical Center in the Netherlands who has called for more monitoring of patients on the new blood thinners, said there had been a “lively discussion” about this issue.
“The company was initially reluctant to recommend anything about monitoring, because they were claiming you no longer have to monitor anymore,” said Dr. ten Cate, who said he had received payments from Boehringer Ingelheim and other companies to speak on such issues, and who also heads a Dutch association of warfarin-testing clinics. “But now, they’ve gradually come back a little bit.”
Others said the newly released documents show that drug makers and regulators had been too eager to approve such powerful drugs without more careful monitoring.
“The one-size-fits-all was a mistake for a drug with this kind of risk,” said Thomas J. Moore, a senior scientist at the Institute for Safe Medication Practices, which keeps track of safety reports submitted to the F.D.A. He rated anticoagulants — including warfarin and Pradaxa — as the most serious safety problem in 2011 and 2012. He said Pradaxa has been cited in more than 1,000 deaths reported to the agency through the end of 2012.

Monday, 3 February 2014

Pharma blog: Can sleeping too much cause chronic diseases?

Pharma blog: Can sleeping too much cause chronic diseases?: “People who get more than 10 hours a night have an increased risk of heart disease, diabetes and obesity,” the Mail Online warns. The stud...

Can sleeping too much cause chronic diseases?

“People who get more than 10 hours a night have an increased risk of heart disease, diabetes and obesity,” the Mail Online warns. The study this news is based on also found that those who don’t get enough sleep have an increased risk of disease.
The study in question used survey data, collected via telephone, from more than 50,000 middle aged and older adults from 14 US states. The survey included questions on whether the person had ever been told they had heart diseasestroke or diabetes and how many hours sleep they normally got.
The researchers found either sleeping more or less than the recommended amount (seven to nine hours) was associated with increased likelihood of having these three chronic diseases. 
A limitation of this study is its design; it was a cross sectional study where data is gathered at a single point in time. This means it cannot show a direct cause and effect relationship between sleep and disease risk. For example, it could be the case that the symptoms of heart disease were causing some people to sleep more, rather than sleeping more leading to heart disease.
The study also failed to assess the various other factors that could influence both chronic disease risk and sleep history, such as lifestyle (for example, smoking, alcohol, physical activity and diet), family history, and other diagnosed physical and mental health illness.
Overall, the study supports current recommendations on optimal sleep duration, but does not prove that less than or more than this directly causes chronic disease. So, occasionally having a long snooze is probably not something you should lose any sleep over.

Where did the story come from?

The study was carried out by researchers from the Centers for Disease Control and Prevention, Atlanta, US, and received no external funding.
The study was published in the peer-reviewed medical journal Sleep.
The Mail Online accurately reports the main findings of this study but does not discuss its inherent limitations – that it cannot prove any direct cause and effect relationship between sleep duration and disease risk.

What kind of research was this?

This was a cross sectional study which used survey data collected from more than 50,000 middle aged and older adults from 14 US states. The data examined their health and lifestyle factors, and the researchers aimed to look at the relationship between sleep duration, heart disease and diabetes, and to see how this relationship was influenced by obesity and mental health.
The researchers suggested that short sleep of six or fewer hours per night, due to our work and lifestyles, may be associated with several chronic diseases, though the underlying mechanisms are poorly understood. The researchers’ theory is that short sleep may influence our metabolism and insulin regulation and increase risk of weight gain. However, these are only theories.
The main difficulty with this study design is that it is cross sectional so cannot prove cause and effect and say that it is the duration of sleep that is directly causing the risk of these diseases. A multitude of biological, health and lifestyle factors may be confounding the relationship and having an influence on both a person’s sleep duration and their risk of the chronic diseases studied.

What did the research involve?

The research used data from the 2010 Behavioural Risk Factor Surveillance System survey, which uses random-digit dialling to survey people in all 50 US states. The overall response rate in 2010 was 52.7% of those invited to participate. In addition to interviewer-administered questionnaires about health-related behaviours and chronic diseases, 14 of the states surveyed in 2010 also completed the optional sleep module.
Presence of chronic disease was assessed through an affirmative ‘yes’ response to the question of whether they had ever been told by a health professional that they had a history of coronary heart disease (such as heart attack or angina) stroke or diabetes. People who said ‘don’t know’ or ‘not sure’ were classed as not having the conditions.
People who also said they had pre-diabetes or borderline diabetes (raised blood glucose but not meeting diagnostic criteria for diabetes) were not classed as having diabetes.
Because of the low prevalence of these diseases among adults younger than 44 years old, the researchers restricted their study to adults aged 45 years or older.
Sleep duration was ascertained by asking ‘On average how many hours of sleep do you get in a 24 hour period?’ Responses were rounded to the nearest hour. The optimal amount of sleep recommended varies by different organisations, but tends to be either seven to eight or seven to nine hours a night for an adult. Therefore the researchers considered short sleep duration to be six or fewer hours, and long duration to be 10 or more hours a night.
When analysing the relationship between sleep duration and the chronic diseases assessed, researchers took into account assessed variables of age, ethnicity, education, body mass index (BMI) (calculated from self-reported height and weight), and ‘frequent mental distress’ (FMD).
FMD was assessed by asking participants ‘about your mental health, which includes stress, depression and problems with emotions, for how many days during the past 30 was your mental health not good?’
Those who answered 14 or more days to this question were defined as having FMD.

What were the basic results?

Complete 2010 survey data was available for 54,269 adults aged 45 or older in the 14 states. A third of these people were 65 years or older, half were women and three quarters were of white ethnicity.
Around a third (31.1%) of participants reported sleeping for six or fewer hours each night, while only 4.1% slept for 10 or more hours a night.
Prevalence of the chronic diseases among all participants was:
  • coronary heart disease: 10.9%
  • stroke: 4.3%
  • diabetes: 13.2%
Just under a third (28.8%) of participants were obese and 9.7% were defined as having FMD.
Compared to those having the optimal seven to nine hours sleep a night, both shorter duration and longer duration of sleep were associated with significantly higher prevalence of all three chronic diseases, FMD and obesity. The significant associations remained when adjusting for sex, age, ethnicity and education. The size of the risk association with the three diseases altered slightly but remained significant when adjusting separately for obesity, and then for FMD, though no model adjusted for both of these factors at the same time.

How did the researchers interpret the results?

The researchers conclude that their study demonstrates that compared with an optimal sleep duration of seven to nine hours per day, both shorter (six or fewer hours) and longer duration (10 or more hours) were associated with significantly increased risk of coronary heart disease, stroke and diabetes among adults aged 45 years and older.


This 2010 survey data from middle aged and older adults from 14 US states suggests an association between shorter and longer than optimal sleep duration and three chronic diseases. The optimal amount of sleep recommended varies by different organisations, but tends to be either seven to eight or seven to nine hours a night for an adult.
However, though the study benefits from its large sample size of over 50,000 adults it has significant limitations.

Cross sectional study design

Most importantly, the cross sectional study design which has assessed sleep duration and disease presence at the same time cannot prove cause and effect. It is not possible to say whether the shorter or longer sleep preceded or followed the onset of these conditions.

Self reported responses

All responses were self-reported. This included both the presence of diseases (which were not confirmed by medical records), sleep duration (which for many people may only be an estimate and may not remain the same all the time), and obesity (assessed though self-reported height and weight, which may be inaccurate).

Likely influence of confounding factors

It is possible that if a true relationship exists between sleep duration and these three chronic diseases, it is not a direct effect of sleep duration but is being influenced by confounding from other biological, health and lifestyle factors. The main factors that the researchers considered as potential confounders (aside from sex, age, ethnicity and education) were obesity and their measure of ‘frequent mental distress’.
As stated, obesity was from self-reported measures and may not be accurate, and similarly the researchers’ method of assessing FMD by a single question may not give a reliable indication of the person’s psychological health.
The researchers adjusted their analyses for obesity and FMD independently, though not together, but did not, or could not, measure the extent of other factors that may be confounding the relationship – for example, other lifestyle factors such as smoking, diet, alcohol and physical activity, family history, and presence of other diagnosed physical or mental health illnesses. 

Saturday, 1 February 2014

Ranbaxys Toansa plant products banned by USFDA due to data integrity issues

Ranbaxys Toansa plant products banned by USFDA due to data integrity issues

Ranbaxy Laboratories had entered into a $500-million settlement in May last year after allegations of fake test results and selling of adulterated products. Now, the USFDA has banned products from Toansa plant of Ranbaxy Laboratories which has affected Ranbaxy with regards to selling products in the US market. Data integrity violations have been cited by the US regulator leading to ban at read more

Admissions notification for various Quality Council of India (QCI), Government of India Approved and Certified and Industry Endorsed Programmes in 1) Pharma Good Manufacturing Practices 2) QA & QC 3) Regulatory Affairs and also in 4) Clinical Research 5) Good Laboratory Practice & 6) IPR(E cum distance learning) VIEW NOW

FDA notes flies in sample storage room at Toansa plant

The US Food and Drug Administration (FDA) has presented a final guidance aiming to clarify the need for information given in the Dear Doctor or ‘Dear Healthcare Provider’ (DHCP) letters. These letters are bulk mailers and are usually sent out to inform about an adverse reaction or a problem with the usage of a drug or medicinal product.Such letters are read more

EU, UK and Aussie regulators focus on Ranbaxys Toansa plant

Fourth warning letter in the last 9 months has been issued to NVN Therapeutics, a manufacturer of a medical food, by the US Food and Drug Administration (FDA). As given by the FDA guidelines, medical foods are not intended to be a part of general diet like consuming vegetables and fruits to reduce the risk of obesity or read more

Indian drug regulator too watches for Ranbaxys Toansa plant

With a host of activities occurring around Ranbaxys Toansa plant at Punjab, the Indian drug regulator, Drug Controller General of India (DCGI), also felt the need to take active involvement. The drug regulator has ordered the company to provide with complete details and explanation regarding the violation of good manufacturing practice (GMP) standards at 

USFDA issues warning letters for GMP violations

There has been a general increase in warning letters issued by USFDA, for violations of good manufacturing practice (GMP) standards. Recently, USFDA conducted inspections at some food and drug manufacturing sites and issued warning letters to the companies. One warning letter was issued to Gadre Marine Export read more

Quinapril tablets recalled by Lupin Pharmaceuticals from the US market

After failing the impurity specification test for multiple lots of quinapril tablets, the US subsidiary of Lupin Pharmaceuticals has voluntarily recalled quinapril tablets from the US market under class-II. As given by USFDA, in class-II recall, the use of a violative product during manufacturing can cause temporary or adverse health consequences that are reversible and