Target Health ( a full service e*CRO, is committed to serve the pharmaceutical community through knowledge, experience, technology and connectivity. Target Health strives to optimize the life cycle of drugs, biologics and devices with expertise, leadership, innovation and teamwork. Target Health Inc. has fulltime staff dedicated to all aspects of Regulatory Affairs, Clinical Research, Biostatistics, Data Management, Strategic Planning and Drug and Device Development. Target Health is committed to the paperless clinical trial and has developed a full suite of eClinical Trial software including:

1) Target e*CRF® (EDC Made Simple)

2) Target e*CTMS™

3) Target Document®

4) Target Encoder®

5) Target e*Pharmacovigilance™

6) Target e*Monitoring™

7) Target Newsletter®

8) Target e*CTR™ (eSource, electronic medical record for clinical trials).

Target Health’s Pharmaceutical Advisory Dream Team assists companies in strategic planning from Discovery to Market Launch. Let us help you on your next project.

261 Madison Avenue
24th Floor
New York, NY 10016
Phone:  (212) 681-2100 ; Fax  (212) 681-2105
Ms Joyce Hays, CEO
Dr. Jules T. Mitchel, President

©2013 Target Health Inc. All rights reserved

Ask Us How to Improve Quality and Save Dollars, Euros, etc. Using Our eSource Solution to the Paperless Clinical Trial


In addition to 2 current development programs (1 US IND and 1 joint US and Canadian INDs), Target eClinical Trial Record (Target e*CTR™), the eSource solution for clinical trials, will be initiated in 3 new US IND drug development programs in Q1 2013, and in 2 unique US development programs in Q2 2013 (1 device IDE and 1 drug IND).


Currently, there have been 7 protocols initiated using Target e*CTR fully integrated with Target e*CRF®. Each protocol also used Target Monitoring Reports™ and Target e*Pharmacovigilance™ for SAE management, each also fully integrated with Target e*CRF®. All of the protocols have also used Target Document for the eTrial Master File (eTMF). It has been an extraordinary experience with onsite monitoring being reduced by 65% and yes, major improvements in quality and enormous cost savings.


Formal meetings have already been held with the US FDA and Health Canada.


For more information about Target Health contact Warren Pearlson (212-681-2100 ext. 104). For additional information about software tools for paperless clinical trials, please also feel free to contact Dr. Jules T. Mitchel or Ms. Joyce Hays. The Target Health software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website at

Are Humans Simply More Evolved Neanderthals?


What will it take for experts to agree on whether Neanderthals (foreground) and modern humans are one and the same species? Photo credit: Copyright Frank Franklin II/AP/Corbis



Over the past 15 years, Svante Paabo, a geneticist at the Max Planck Institute of Evolutionary Anthropology, and his colleagues have uncovered an entirely new source of evidence about the nature of Neanderthals: their DNA. Starting with those 1) ___ from the Neander Valley, they extracted bits of genetic material that had survived tens of thousands of years. Eventually, they were able to assemble the fragments into the entire Neanderthal genome.


It’s clearly different from the genome of any human alive today, sprinkled with many distinctive mutations. These mutations accumulated in a clock-like way, and by tallying them up, Paabo and his colleagues estimate that Neanderthals and humans share a common ancestor that lived 800,000 years ago. It’s possible that the 2) ___ of Neanderthals expanded out of Africa then, while our own ancestors stayed behind. That’s a long time – long enough to reasonably ask if humans and Neanderthals are indeed two separate species. Old species split into new ones when some of their members get isolated from the rest. If a river cuts the range of a species of frog in two, for example, the frogs on one side of the river may only be able to mate with one another. Each population will 3) ___ along its own path. If they are isolated long enough, they will have trouble interbreeding. They may even be unable to 4) ___ at all.


From these facts of evolution, the biologist Ernst Mayr developed what came to be known as the Biological Species Concept in the 1940s – namely, a species is made up of members of populations that actually or potentially interbreed in nature. Experiments on living animals have shown that barriers to this interbreeding can arise in tens of thousands, or even just thousands, of years.


Once the Neanderthal lineage left Africa 800,000 years ago, did 5) ___ and Neanderthals have enough time to become unable to interbreed? Paabo’s research provides an answer: no.


Does the late Ernst Mayr’s notion of what constitutes a species, which held sway for many decades, need to be scrapped or substantially revised? Many biologists believe so. Photo credit: copyright Rick Friedman/Corbis



Europeans and Asians carry with them a small portion of DNA inherited from Neanderthals – while Africans do not. The best explanation for our mixed genomes is that after humans expanded out of Africa, they encountered Neanderthals and interbred. Comparing the different Neanderthal-derived genes in different people, Paabo and his colleagues estimate that this encounter occurred around 6) ___ years ago. The tiny amount of Neanderthal DNA has been interpreted by some scientists as evidence that Neanderthals rarely mated with humans – perhaps just once, in fact. But as scientists sequence more genomes from more human populations, they’re exploring the possibility that our ancestors mated with Neanderthals several different times.


The presence of 7) ___ from Neanderthals in human genomes is compelling evidence that humans and Neanderthals could mate and produce fertile offspring. If we stick to the Biological Species Concept, then we are a single species, as Schaafhausen originally thought. But some scientists reject this argument. They think that Mayr’s Biological Species Concept has worn out its usefulness.


Homo neanderthalensis and Homo sapiens endured at least until the Neanderthals became 8) ___. With the advent of gene sequencing, scientists have found that many animal species regularly interbreed. It’s easy for any safari tourist to tell the difference between olive baboons and yellow baboons that live in Kenya, for example. And yet the two 9) __ regularly produce hybrids in the places where their species overlap, and they’ve been doing it for a long time.


Populations of the same species that a river or other barrier divides can become unable to breed successfully with each other. Such an inability never occurred between Neanderthals and humans, who bred successfully at least once. Photo credit: copyright thobo/iStockphoto



So why haven’t the two baboon species merged into a single hybrid olive-yellow species? The baboons produced by interbreeding may not survive as well as purebred ones. They produce fewer offspring of their own, and so the 10) ___ from one species don’t spread easily in the other. Thus, despite interbreeding – breaking Ernst Mayr’s rule, in other words – the olive and yellow baboons endure as separate species. Perhaps humans and Neanderthals were the same: They only interbred rarely, and when they did, the 11) ___ children couldn’t fuse the two kinds of humans together. That may be why human and Neanderthal fossils remained so different. William King would probably have been horrified at the notion of human beings having intercourse with Neanderthal “brutes.” But despite this intermingling, Homo neanderthalensis and Homo sapiens endured – at least until the Neanderthals became extinct, and we 12) ___.

Source:  Decoding Neanderthals — By Carl Zimmer


ANSWERS: 1) fossils; 2) ancestors; 3) evolve; 4) interbreed; 5) humans; 6) 40,000; 7) DNA; 8) extinct; 9) species; 10) genes; 11) hybrid; 12) survived

Are Neanderthals Human?


Do Neanderthals belong within Homo sapiens? Paleoanthropologists cannot agree. Here, a skull cast of the La Chapelle-aux-Saints Neanderthal discovered in 1908. Photo credit: copyright Stefano Bianchetti/Corbis



In August 1856, in the German valley of Neander – Neanderthal in German – men cutting limestone for the Prussian construction industry stumbled upon some bones in a cave. Looking vaguely human, the bones – a piece of a skull, portions of limbs, and fragments of shoulder blades and ribs – eventually made their way to an anatomist in Bonn named Hermann Schaafhausen.


Schaafhausen pored over the fossils, observing their crests and knobs. He noticed that the bones had the overall shape you’d expect from a human skeleton. But some bones had strange features, too. The skullcap, for example, sported a heavy brow ridge, hanging over the eyes like a boney pair of goggles. It was, at once, human and not. The Neanderthal Man challenged Schaafhausen with a simple yet profound question: Was it a human, or did it belong to another species?


It’s been over 150 years since the bones first emerged from the Neander Valley – a time during which we’ve learned a vast amount about human evolution. Today, scientists can even scan the genomes of Neanderthals who died 50,000 years ago. And yet the debate still rages. It’s a debate that extends beyond Neanderthals, forcing us to ask what it means to be a species at all. The Neander Valley bones were a sensation as soon as Schaafhausen published his report on them in 1857, because nothing like them had been seen before. Earlier in the 1800s, cave explorers had found ancient human bones, sometimes lying next to fossils of cave bears and other extinct animals. Naturalists had a hazy sense from such bones that humanity had been around for quite a long time. But the idea that humans – or any other species – had evolved was scandalous. Darwin would not publish The Origin of Species for another two years. Instead, naturalists saw humans as a species distinct from chimpanzees, gorillas, and all other primate species. We were distinct today, and we had been distinct since creation.


The youngest Neanderthal fossils date to 28,000 years ago.


Within the human species, European anatomists divided people into races. They often ranked Europeans as the noblest race, considering the others barely better than apes. To justify this racist view of humanity, anatomists searched for clear-cut differences between the skeletons of different races – the size of skulls, the slopes of brows, the width of noses. Yet their attempts to neatly sort people into groups were bedeviled by the blurry variations in our species. Within a single so-called race, people varied in color, height, and facial features. Schaafhausen knew, for example, about a skull dug up from an ancient grave in Germany that “resembled that of a Negro,” as he wrote.


A barbarian (with sword) attacking a Roman legionary in a second-century relief. Neanderthals wouldn’t have been out of place amongst such savage sorts, Schaafhausen believed. Photo credit: copyright The Gallery Collection/Corbis



On this confusing landscape Schaafhausen tried find a place for the Neanderthal Man. He decided that its heavy brow didn’t disqualify it as a human. To back up this diagnosis, he relied on stories of ancient European savagery. “Even of the Germans,” Schaafhausen wrote in his 1857 report on the Neander Valley bones, “Caesar remarks that the Roman soldiers were unable to withstand their aspect and the flashing of their eyes, and that a sudden panic seized his army.” Schaafhausen searched historical records for other clues of Europe’s monstrous past. “The Irish were voracious cannibals, and considered it praiseworthy to eat the bodies of their parents,” he wrote. In the 1200s, ancient tribes in Scandinavia still lived in the mountains and forests, wearing animal skins, “uttering sounds more like the cries of wild beasts than human speech.” Surely, in such a savage place, this heavy-browed Neanderthal would have fit right in. When Schaafhausen published his report, many other naturalists tried to make sense of the bones for themselves. After Darwin published his theory of evolution in 1859, new possibilities arose: Perhaps humans evolved from Neanderthals, or perhaps they were both descended from a common ancestor.


Thomas Huxley, Darwin’s great champion in England, argued that Neanderthals were human, pointing to the thick foreheads of living Australian Aborigines. William King, an Irish geologist, disagreed. In an 1864 paper, “The Reputed Fossil Man of the Neanderthal,” he pointed to a long list of traits that separated it from living humans – from its tightly curved ribs to the massive sinuses in its skull. Its braincase was so ape-like that it could not house a human-like brain.


Australian Aborigines have a prominent brow ridge, a fact that helped lead Thomas Huxley to argue that Neanderthals were indeed human.



“I feel myself constrained to believe that the thoughts and desires which once dwelt within it never soared beyond those of a brute,” King wrote. From all this evidence, King concluded that the Neanderthal Man was not simply an ancient European, as Schaafhausen had thought. It was a separate species. He even gave that species a name: Homo neanderthalensis. King was certainly right that Neanderthals were distinct from living humans. Subsequent generations of fossil-hunters have found remains of Neanderthals from Spain to Israel to Russia. The youngest Neanderthal fossils date to 28,000 years ago. The oldest ones date back over 200,000 years. Like the original Neanderthal Man, they were stocky, with a heavy brow ridge and other singular traits. We can’t know exactly what thoughts and desires soared in their heads, but they certainly left behind some telling clues – carefully engineered spear blades and stone knives; painted shells that might have been used as jewelry. Neanderthals endured the comings and goings of ice ages in Europe and Asia, hunting for reindeer, rhinoceroses, and other big game.


As the fossils have emerged, paleoanthropologists have revisited the question of whether Neanderthals are part of our own species – call them Homo sapiens neanderthalensis – or a separate Homo neanderthalensis. Some researchers argued that Neanderthals belonged to a single species of humans stretching across the Old World, one that evolved over the past million years from small-brained hominids into our big-brained form.


Do Europeans, Africans and Asians carry a small portion of DNA inherited from Neanderthals? Some researchers challenged this view. They pointed out that for thousands of years, Europe was home to the burly Neanderthals as well as slender humans. Neanderthals didn’t give rise to living Europeans, these scientists argued; they were replaced by immigrants expanding out of Africa—perhaps even outcompeted into extinction.

Source:  Decoding Neanderthals — By Carl Zimmer

NIH Urges Dilated Eye Exams to Detect Glaucoma


Glaucoma is a major cause of vision loss in the United States and it is becoming more prevalent as our population ages. About 2.7 million Americans 40 and older have primary open-angle glaucoma, the most common form, and this number is expected to grow. Several large studies have shown that eye pressure is a major risk factor for optic nerve damage. In open-angle glaucoma pressure inside the eye rises to a level that may damage the optic nerve. When the optic nerve is damaged from increased pressure, vision loss may result. “Vision Problems in the U.S.,” a report released in 2012, by Prevent Blindness America and The National Eye Institute (NEI), predicts that by 2030 the disease will affect 4.2 million Americans.


The NEI, a part of the National Institutes of Health, observes Glaucoma Awareness Month each January by encouraging Americans at higher risk for glaucoma to schedule a comprehensive dilated eye exam and to make a habit of doing so every one to two years. While anyone can get glaucoma, people at higher risk include African Americans age 40 and over; adults over the age of 60, especially those who are Mexican American; and people who have a family history of the disease.


Glaucoma can be detected in its early stages through a comprehensive dilated eye exam before vision loss occurs. During this exam, drops are placed in the eyes to dilate, or widen, the pupils. This allows an eye care professional to examine the optic nerve for signs of damage and other possible problems. An eye pressure test alone is not enough to detect glaucoma. People in the higher risk categories should not wait until they notice a problem with their vision to have an eye exam. Primary open-angle glaucoma often has no symptoms in its early stages, so people may not know they have glaucoma until they start to have noticeable vision loss.


NEI leads the nation’s vision research efforts and is committed to finding better prevention, detection, and treatment of eye diseases and disorders. In 2012, NEI invested $71 million in a wide range of studies to understand causes and potential areas of treatment for glaucoma.


The broad scope of NEI-funded glaucoma research ranges from gene therapy to stem cells, drug treatments, vaccines to protect the optic nerve cells, advanced imaging tools to view the retina and optic nerve, and new techniques to study glaucoma disease mechanisms, such as new mouse models that simulate glaucoma. These models enable scientists to study how increased eye pressure causes optic nerve cell death.

Is Alzheimer’s Disease Type 3 Diabetes?


Type 1 diabetes, in which the immune system destroys insulin-producing cells in the pancreas, accounts for about 10% of all cases. Type 2 diabetes is chronic or environmental, and it’s especially prevalent in populations that overconsume hyperprocessed foods, like ours. It’s tragically, increasingly common – about a third of Americans have diabetes or pre-diabetes – which is treatable but incurable. It causes cells to fail to retrieve glucose from the blood, either because the pancreas isn’t producing enough insulin or the body’s cells ignore that insulin.


If the rate of Alzheimer’s rises in lockstep with Type 2 diabetes, which has nearly tripled in the United States in the last 40 years, we will shortly see a devastatingly high percentage of our population with not only failing bodies but brains. Even for the lucky ones this is terrible news, because 5.4 million Americans (nearly 2%, for those keeping score at home) have the disease, the care for which – along with other dementias – will cost around $200 billion this year. That’s more than the $150 billion we spend annually on obesity-related illnesses. So the financial cost of the obesity pandemic just more than doubled. More than 115 million new cases of AD are projected around the world in the next 40 years, and the cost is expected to rise to more than a trillion of today’s dollars.


Interest in characterizing the role of impaired insulin actions in Alzheimer’s disease (AD) and vascular dementia was originally reported in an article published in 2005 in the Journal of Alzheimers Disease (2005 7:45-61). The article detailed about what was currently known about insulin, insulin-like growth factor type I (IGF-I) and IGF-II proteins and their corresponding receptors in the brain, and delineated the major controversies pertaining to alterations in the expression and function of these molecules in AD. The various experimental animal models generated by over-expression, mutation, or depletion of genes that are critical to the insulin or IGF signaling cascades were summarized, noting the degrees to which they reproduce the histopathological, biochemical, molecular, or behavioral abnormalities associated with AD. Although no single model was determined to be truly representative of AD, depletion of the neuronal insulin receptor and intracerebroventricular injection of Streptozotocin reproduce a number of important aspects of AD-type neurodegeneration, and therefore provide supportive evidence that AD may be caused in part by neuronal insulin resistance, i.e. brain diabetes. The extant literature did not resolve whether the CNS insulin resistance in AD represents a local disease process, or complication/extension of peripheral insulin resistance, i.e. chronic hyperglycemia, hyperinsulinemia, and Type 2 diabetes mellitus. The available epidemiological data are largely inconclusive with regard to the contribution of Type 2 diabetes mellitus to cognitive impairment and AD-type neurodegeneration. A major conclusion drawn from this review is that there is a genuine need for thorough and comprehensive study of the neuropathological changes associated with diabetes mellitus, in the presence or absence of superimposed AD or vascular dementia. Strategies for intervention may depend entirely upon whether the CNS disease processes are mediated by peripheral, central, or both types of insulin resistance.


The study analyzed insulin and insulin receptor function in 45 postmortem brains from either normal elderly patients or AD patients at various stages of disease. They found that insulin expression declined in step with Braak stages, the standard system of neurodegeneration classification. In the most advanced stage of AD, insulin receptors were nearly 80% lower than in a normal brain, and what’s more, the ability of insulin and its related growth factor IGF-I to bind to corresponding receptors also diminished, creating a cellular resistance to these proteins that ultimately led to cell death.


We all need insulin. In non-diabetics, it’s released to help cells take in the blood sugar (glucose) they need for energy. But the cells can hold only so much; excess sugar is first stored as glycogen, and – when there’s enough of that – as fat. Insulin not only keeps the blood vessels that supply the brain healthy, it also encourages the brain’s neurons to absorb glucose, and allows those neurons to change and become stronger. Low insulin levels in the brain mean reduced brain function.


When the insulin demand is high, as it does when you drink sugar-sweetened beverages and repeatedly eat junk food, the cells are overwhelmed, and say, “enough.” They become resistant. This makes the insulin even more insistent and, to make matters worse, all those elevated insulin levels are also bad for blood vessels.


Please check out these links: 1. Detailed summary by Dr. de la Monte: Alzheimer’s: Diabetes of the Brain?  2. Rhode Island Hospital: A Link Between Brain Insulin Resistance and Neuronal Stress in Worsening Alzheimer’s Disease 3. NIH: Relative Intake of Macronutrients Impacts Risk of Mild Cognitive Impairment or Dementia and The Whitehall II Cohort Study;

NIH Launches Collaborative Effort to Find Biomarkers for Parkinson’s Disease


Parkinson’s disease (PD) is a movement disorder that affects about 1 million people in the US. Symptoms of the disease get worse over time, and include uncontrollable shaking, rigidity, slowed movements and impaired balance. Inside the brain, there is a progressive loss of cells in a motor control region called the substantia nigra, and an accumulation of protein-filled structures called Lewy bodies. Lewy bodies and other telltale signs cannot be observed until after death. Biomarkers could be used to detect and monitor the disease much earlier, perhaps even before symptoms appear. This could improve the success of existing therapies and help researchers test new ones in clinical trials.


Biomarkers can include changes in body chemistry or physiology, in genes and how they are regulated, and even subtle changes in a person’s behavior. For example, certain antibodies in the blood can be biomarkers for different types of infection. For PD, there are no proven biomarkers. This lack of biomarkers for PD has been a major challenge for developing better treatments. The Parkinson’s Disease Biomarkers Program (PDBP) supports efforts to invent new technologies and analysis tools for biomarker discovery, to identify and validate biomarkers in patients, and to share biomarker data and resources across the PD community. The initiative also aims to accelerate the search for biomarkers that can be used to predict, diagnose or monitor PD.


The range of potential biomarkers for PD is vast, and there have been promising leads. Some laboratories are investigating the use of non-invasive imaging to detect changes in brain function or biochemistry. Several studies have tentatively linked the disease with changes in proteins or other molecules in blood, urine, or in the cerebrospinal fluid (CSF) that bathes the brain and spinal cord.

TARGET HEALTH excels in Regulatory Affairs. Each week we highlight new information in this challenging area


FDA and Sub-Saharan Partners Protecting Public Health


FDA and its partners in Sub-Saharan Africa have made great strides in improving the oversight of the clinical trials of medical products in development, an important advance in protecting public health in both the U.S. and Africa. This is important not only to protect the Africans who are participating in these tests of medical products, but also because the FDA and other regulatory authorities must rely on the results of these studies when reviewing marketing applications for the products.


FDA’s Office of International Programs (OIP) established its Sub-Saharan Africa Post in Pretoria, South Africa, in June 2011 and has been building regional relationships that allow the sharing of information about FDA policies and procedures, and to better understand local regulatory landscapes. This has not been an easy task in a vast region of 54 countries with varying degrees of regulatory strengths and capabilities.


However, the collaboration with the Southern Africa Development Community (SADC), which represents 15 African nations, has allowed FDA to strategically engage in strengthening regulatory capacity in the area of Good Clinical Practices (GCPs) and clinical trial inspections. These practices, and the inspections to ensure that they are followed, are designed to protect the integrity of data produced by the trial and the safety of its participants.


This activity has given expertise to regulators who did not think their knowledge base was extensive enough to audit (monitor) and inspect clinical trials. Regulators in countries that once did not audit clinical trials are now doing so. With more than 2,000 clinical trials being conducted in Africa – over half of them in South Africa – this has become a momentous public health achievement.


The Sub-Saharan Africa Post conducted a successful FDA/SADC Good Clinical Practice Inspection training from August 24-28, 2012, in Lusaka, Zambia. Thirty six drug regulators from 13 SADC countries participated, including Angola, Botswana, Lesotho, Malawi, Mauritius, Mozambique, Namibia, Seychelles, South Africa, Swaziland, Tanzania, Zambia and Zimbabwe. This was the third in an FDA training series – typically offered in three to four phases – to develop trainers who have expertise in clinical practices and inspection. These individuals will also be prepared to train others within their agencies and the regulated community.


This particular workshop was designed to reinforce lessons learned and provide additional inspectional experience for those who completed workshops in the first two training phases in Botswana in 2010 and in Pretoria in 2011. The goals of Phase 3 include reviewing core knowledge and skills, preparing inspection reports and inspectional observations; acquiring additional mock inspection experience at clinical investigator sites; gaining experience with new types of study protocols; and promoting regional networking.


These countries continue to make substantial progress in the oversight of clinical trials. For example, at the onset of the first training, only three of 13 participating countries were involved in how clinical trials are conducted. There are now an additional two countries conducting oversight, with others poised to start soon. Other milestones from training include important advances towards systematic oversight in Botswana, Mauritius, Swaziland, Tanzania, Zambia and Zimbabwe.

Coconut Oil-Poached Tilapia, So Easy a Caveman Could Do It


Poached Tilapia with wilted baby spinach, pear & carrot slaw




  • 3 or 4 6-7oz Tilapia fillets
  • 2 garlic cloves, juiced
  • 1/3 cup cilantro, chopped
  • Juice of 1 lime, plus teaspoon lime zest or to your taste
  • 1/2 cup Extra Virgin Coconut Oil (make oil 1/4” deep in your pan)
  • Pinch of Kosher or sea Salt (optional)
  • Parsley for garnish, lemon wedges




  1. Use a pan with cover, preferably a glass cover.
  2. Heat coconut oil and salt over medium-low heat until hot, just starting to bubble but not a rolling boil, keep at a simmer. Juice the 2 garlic cloves right into the pan. Add the lime and lime zest, and the chopped cilantro. Stir everything.
  3. Add tilapia to the pan.
  4. Cover and cook until the top edges of the fish are opaque, 7 to10 minutes. Flip over each piece of fish. Cook another 5 minutes until the fish is fully cooked and opaque throughout.
  5. Serve over jasmine or basmati rice, with wilted baby spinach and spoon some of the pan juice over each serving of tilapia. Sprinkle with some extra cilantro or fresh parsley and add some lemon wedges.


Be sure to serve this tilapia with warm grainy bread or rolls to sop up the juice. Make a simple tossed salad or (as you see in the photo) a simple fruit and carrot slaw. Or, try the easy cashew dressing in this posting, served over endive pieces (not too small), with some dried cranberries, or dried blueberries, or dried mulberries sprinkled over the endive.  Finally, a few chopped cashews on top of the dressing.


We would bring out chilled Sauvignon Blanc for this occasion.



What Does Target Health Inc. Do For a Living?


Several times a year we are asked what Target Health Inc. does for a living. So here is a brief summary.


In 2013, Target Health will celebrate its 20th year as a New York City-based, full-service e*CRO with full-time staff dedicated to all aspects of the “paperless clinical trial” complementing our expertise in:


1. Drug and Device Strategic Development Planning

2. All aspects of Regulatory Affairs including eCTD submissions

3. Clinical Research Management

4. Biostatistics

5. Data Management

6. Internet-based clinical trials (Target e*CRF®)

7. Medical Writing


In addition to Target e*CRF, we also provide fully validated software for clinical trials including:


1. Target e*CTR® (eSource eClinical Trial Record; fully integrated with Target e*CRF )

2. Target Encoder®(coding MedDRA and WHODrug)

3. Target e*Pharmacovigilance™ (Form 3500A and CIOMS1; fully integrated with Target e*CRF)

4. Target Document® (eTMF)

5. Target e*CTMS® (Clinical Trial Management System)

6. Target Monitoring Reports (fully integrated with Target e*CRF)

7. Target Newsletter™ (fully integrated with Target e*CRF)


For more information about Target Health contact Warren Pearlson (212-681-2100 ext. 104). For additional information about software tools for paperless clinical trials, please also feel free to contact Dr. Jules T. Mitchel or Ms. Joyce Hays. The Target Health software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website at

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