Target Health has the best strategic regulatory group in the US. Led by Glen Park, PharmD with direct support from Jules T. Mitchel, PhD, Target Health represents over 30 companies at FDA from Denmark, France, Israel, Korea, Sweden, Switzerland and the US. Target Health is headquartered on Madison Avenue in New York City, so hard work is always combined with NYC culture, dynamism and diversity.


Target Health also does paperless regulatory submissions with a great team led by Mary Shatzoff.  Mary is our in-house chemist, and our clients always appreciate her attention to detail. Since 1993, Target Health has played major roles in the approval of over 30+ drugs, biologics and devices and more to come this year.


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

How Exercise Fuels the Brain


Shannon Stapleton/Reuters – Does exercise keep your brain running?



Moving the 1) ___ demands a lot from the brain. Exercise activates countless neurons, which generate, receive and interpret repeated, rapid-fire messages from the nervous system, coordinating 2) ___ contractions, vision, balance, organ function and all of the complex interactions of bodily systems that allow you to take one step, then another. This increase in brain activity naturally increases the brain’s need for nutrients, but until recently, scientists hadn’t fully understood how neurons fuel themselves during exercise. Now a series of animal studies from Japan suggest that the exercising 3) ___ has unique methods of keeping itself fueled. What’s more, the finely honed energy balance that occurs in the brain appears to have implications not only for how well the brain functions during exercise, but also for how well our thinking and memory work the rest of the time.


For many years, scientists had believed that the brain, which is a very hungry organ, subsisted only on 4) ___, or blood sugar, which it absorbed from the passing bloodstream. But about 10 years ago, some neuroscientists found that specialized cells in the brain, known as astrocytes, that act as support cells for neurons actually contained small stores of glycogen, or stored carbohydrates. And glycogen, as it turns out, is critical for the health of 5) ___ throughout the brain.


In petri dishes, when 6) ___, which do not have energy stores of their own, are starved of blood sugar, their neighboring astrocytes undergo a complex physiological process that results in those cells’ stores of glycogen being broken down into a form easily burned by neurons. This substance is released into the space between the cells and the neurons swallow it, maintaining their energy levels. But while scientists knew that the brain had and could access these 7) ___ stores, they had been unable to study when the brain’s stored energy was being used in actual live conditions, outside of petri dishes, because brain glycogen is metabolized or burned away very rapidly after death; it’s gone before it can be measured.


That’s where the Japanese researchers came in. They had developed a new method of using high-powered microwave irradiation to instantly freeze glycogen levels at 8) ___, so that the scientists could accurately assess just how much brain glycogen remained in the astrocytes or had recently been used. In the first of their new experiments, published last year in The Journal of Physiology, scientists at the Laboratory of Biochemistry and Neuroscience at the University of Tsukuba gathered two groups of adult male rats and had one group start a treadmill running program, while the other group sat for the same period of time each day on unmoving treadmills. The researchers’ aim was to determine how much the 9) ___ of brain glycogen changed during and after exercise. Using their glycogen detection method, they discovered that prolonged exercise significantly lowered the brain’s stores of energy, and that the losses were especially noticeable in certain areas of the brain, like the frontal 10) ___ and the hippocampus, that are involved in thinking and memory, as well as in the mechanics of moving.


The findings of their subsequent follow-up experiment, however, were even more intriguing and consequential. In that study, which appears in this month’s issue of The Journal of Physiology, the researchers studied animals after a single bout of exercise and also after four weeks of regular, moderate-intensity running. After the single session on the 11) ___, the animals were allowed to rest and feed, and then their brain glycogen levels were studied. The food, it appeared, had gone directly to their heads; their brain levels of glycogen not only had been restored to what they had been before the workout, but had soared past that point, increasing by as much as a 60 percent in the frontal cortex and hippocampus and slightly less in other parts of the brain. The astrocytes had “overcompensated,“ resulting in a kind of brain carbo-loading. The levels, however, had dropped back to normal within about 24 hours. That was not the case, though, if the animals continued to exercise. In those rats that ran for four weeks, the “supercompensation“ became the new normal, with their baseline levels of glycogen showing substantial increases compared with the sedentary animals. The increases were especially notable in, again, those portions of the brain critical to learning and memory formation ? the cortex and the 12) ___.


Which is why the findings are potentially so meaningful – and not just for rats. While a brain with more fuel reserves is potentially a brain that can sustain and direct movement longer, it also “may be a key mechanism underlying exercise-enhanced cognitive function,“ says Hideaki Soya, a professor of exercise biochemistry at the University of Tsukuba and senior author of the studies, since supercompensation occurs most strikingly in the parts of the brain that allow us better to think and to remember. As a result, Dr. Soya says, “it is tempting to suggest that increased storage and utility of brain 13) ___ in the cortex and hippocampus might be involved in the development“ of a better, sharper brain. Given the limits of current technologies, brain glycogen metabolism cannot be studied in 14) ___. But even so, the studies’ findings make D.I.Y. brain-fuel supercompensation efforts seem like an attractive possibility. And, according to unpublished data from Dr. Soya’s lab, the process may even be easy. He and his colleagues have found that “glycogen supercompensation in some brain loci“ is “enhanced in rats receiving carbohydrates immediately after exhaustive 15) ___.“ So for people, that might mean that after a run or other exercise that is prolonged or strenuous enough to leave you tired, a bottle of chocolate milk or a banana might be just the thing your brain is needing. Source: The New York Times, 02/24/12, by Gretchen Reynolds


ANSWERS: 1) body; 2) muscle; 3) brain; 4) glucose; 5) cells; 6) neurons; 7) energy; 8) death; 9) level; 10) cortex; 11) treadmill; 12) hippocampus; 13) glycogen; 14) people; 15) exercise

Maurice Ravel – Bolero – Dementia


Maurice Ravel in 1912



Several nights ago a (Charlie Rose) PBS panel discussion led by Eric Kandel MD PhD (Nobel Laureate) and other well-known neuroscientists discussed new positive research in Alzheimer’s disease. This panel mentioned briefly that Maurice Ravel, no doubt, had a form of dementia that was involved in his composition of “Bolero.“


Is Ravel’s Bolero a product of dementia? Is repetition in work symptomatic of Alzheimer’s disease? No one would deny that the sometimes beloved, often reviled Bolero by Maurice Ravel (1875-1937) is repetitive. The French composer himself criticized his most popular work as “a piece for orchestra, without music.“ Could Bolero have been a manifestation of Ravel’s growing dementia?


Originally commissioned in 1928 by ballet dancer Ida Rubinstein as a “choreographed poem,“ the 15-minute work is dominated by a repetitive, hypnotic rhythm. Weaving through these driving beats are two themes, passed around the different sections of the orchestra and each repeated eight times. Changes in the work’s dynamic level – which builds throughout the piece to a bombastic, crashing end, increasing as different instruments carry and pass on the melody – manifest the only variations in the work.


One could argue that Bolero is a great study in the art of orchestration and presents Ravel as a master arranger, making the most of a fleeting musical idea. But in recent years, psychiatric researchers have offered another possible explanation. They suggest that the repetition in Bolero could reflect a manifestation of Alzheimer’s disease, or some other serious mental deterioration. Perseveration, an Alzheimer’s symptom, is the obsession of repeating words or actions, and could have been the mastermind behind Ravel’s infamous masterpiece.


It is known that beginning in 1927 or 1928 – the year he wrote Bolero – Ravel began to experience perplexing health problems. In the last five years of his life, the act of composing became exceedingly difficult and he lost the ability to write out his music. Ravel died in December 28, 1937, nine days after exploratory brain surgery.



Listen to Ravel’s Bolero and tell us what you think.  Joyce Hays, Target Health Inc.

Variation in Brain Development in Infants with Autism


Autism spectrum disorders (ASDs) involve communication and social difficulties as well as repetitive behavior and restricted interests. Many early behavioral signs of ASDs are not apparent until the first year of age. Typically, ASDs are diagnosed at age 3 or older. According to the U.S. Centers for Disease Control and Prevention, ASDs affect 1 of 110 children in the United States.


According to an article published online in the American Journal of Psychiatry (17 February 2012), patterns of brain development in the first two years of life are distinct in children who are later diagnosed with ASD. The study results show differences in brain structure at 6 months of age, the earliest such structural changes have been recorded in ASDs.


The study recorded brain images of 92 infants, all of whom had an older brother or sister with ASDs. Children who have an older sibling with ASDs have an increased risk of developing ASDs. The study used a technique known as diffusion tensor magnetic resonance imaging to track the children’s brain development at 6 months, 1 year and 2 years. As the brain develops, networks of neural circuits known as white matter fiber tracts form connections between the various brain areas. These white matter fiber tracts serve as conduits that convey information throughout the brain.


For the study, specific connections throughout the brain were identified and the strength of these connections was measured. Results showed that when the children were 6 months of age, the white matter connections for children who went on to develop ASDs were initially stronger than for those who did not develop autism. The study also recorded complete sets of images from each child. These sets of images were recorded at three intervals: when the children were 6 months, 12 months, and 24 months of age. In each set of images, 15 such white matter fiber tracts were recorded.


At 6 months, the intensity of these white matter connections was greatest in the group that later developed ASDs. However, by 24 months, the white matter connections in the children with ASDs had apparently failed to keep pace with those of the children who did not develop ASDs. At 12 months and 24 months, the children who did not have ASDs had stronger, more intense connections in 12 of the 15 white matter fiber tracts than did their counterparts who developed ASDs. The authors concluded that these findings indicate that coherent, organized information pathways developed faster in the children who did not have ASDs.


Filed Under News | Leave a Comment

Colonoscopic Polypectomy and Long-Term Prevention of Colorectal-Cancer Deaths


In the National Polyp Study (NPS), it was shown that colorectal cancer was prevented by colonoscopic removal of adenomatous polyps. As a result, a study published in the New England Journal of Medicine (2012;366:687-696), was performed to evaluate the long-term effect of colonoscopic polypectomy in a study on mortality from colorectal cancer.


The analysis included all patients prospectively referred for initial colonoscopy (between 1980 and 1990) at NPS clinical centers who had polyps (adenomas and nonadenomas). The National Death Index was used to identify deaths and to determine the cause of death, with follow-up time was as long as 23 years. Mortality from colorectal cancer among patients with adenomas removed was compared with the expected incidence-based mortality from colorectal cancer in the general population, as estimated from the Surveillance Epidemiology and End Results (SEER) Program, and with the observed mortality from colorectal cancer among patients with nonadenomatous polyps (internal control group).


Results showed that among 2,602 patients who had adenomas removed during participation in the study, after a median of 15.8 years, 1,246 patients had died from any cause and 12 had died from colorectal cancer. Given an estimated 25.4 expected deaths from colorectal cancer in the general population, the standardized incidence-based mortality ratio was 0.47 with colonoscopic polypectomy, suggesting a 53% reduction in mortality. Mortality from colorectal cancer was similar among patients with adenomas and those with nonadenomatous polyps during the first 10 years after polypectomy (relative risk, 1.2).


According to the authors, the findings support the hypothesis that colonoscopic removal of adenomatous polyps prevents death from colorectal cancer.

Ocular Safety of Sildenafil Citrate when Administered Chronically for Pulmonary Arterial Hypertension


One of the advantages of the large pharmaceutical companies is that they have the resources to do extensive clinical trials with their drugs. As drugs come off patent, there are just limited ways to perform additional safety and efficacy studies.


A study published in the British Medical Journal (2012;344:e554) was performed to assess the ocular effects and safety profile of chronic sildenafil oral dosing in patients with pulmonary arterial hypertension. The study was a 12-week, double masked, randomized, placebo controlled, phase III trial, with an open label extension, performed at 53 institutions worldwide.


Participants included 277 adults with idiopathic pulmonary arterial hypertension or pulmonary arterial hypertension associated with connective tissue disease or after congenital heart disease repair (mean pulmonary artery pressure >25 mm Hg; pulmonary capillary wedge pressure <15 mm Hg at rest).


During the double masked study, oral sildenafil 20 mg, 40 mg, or 80 mg or placebo (1:1:1:1) three times daily for 12 weeks was added to baseline drug treatment. In the extension study, the placebo, 20 mg and 40 mg groups received 40 mg three times daily titrated to 80 mg three times daily at week 6. After unmasking, the dose was titrated according to clinical need.


The main outcome measure was ocular safety (ocular examinations, visual function tests, participants’ reports of adverse events, and visual disturbance questionnaire completed by investigators) by treatment group at 12 weeks, 24 weeks, 18 months, and yearly.


Findings of the objective assessments of intraocular pressure and visual function tests (visual acuity, color vision, and visual field) were similar across groups. No clinically significant changes occurred between baseline and 12 weeks, except for an efficacy signal in contrast sensitivity for the sildenafil 40 mg three times daily group. In right eyes, changes in intraocular pressure from baseline to week 12 ranged from a mean of -0.5 mm Hg with placebo, -0.2 mm Hg with sildenafil 40 mg, and -0.1 mm Hg with 80 mg to 0.3 mm Hg with sildenafil 20 mg (the approved dose for pulmonary arterial hypertension). Mean changes from baseline to week 12 in contrast sensitivity in right eyes were -0.02 in the sildenafil 20 mg three times daily group compared with -0.05 in the placebo group (P=0.044).


Percentages of participants with deterioration in visual acuity (Snellen) from baseline to week 12 ranged from 10% (n=7) in the placebo group to 3% (n=2) in the sildenafil 20 mg three times daily group; the same percentages had visual field changes from normal to abnormal during the period in these two groups. The investigators did not deem any findings on color vision assessment to be clinically significant. Findings of the objective assessments in the 40 mg and 80 mg three times daily sildenafil treatment groups and in left eyes were not substantially different, nor were any measures different throughout the open label extension compared with week 12.


Incidence of ocular adverse events reported on the case report forms and assessed by the investigator was low with all doses, but a modest, dose related incidence of chromatopsia, cyanopsia, photophobia, and visual disturbance was reported with 80 mg three times daily consistent with the indicated dosing for erectile dysfunction. Retinal hemorrhages, captured on funduscopy, occurred in 2% (4/207) of sildenafil treated participants and none in the placebo group during the double masked study and in 4% (10/259) during the open label extension.


The authors concluded that sildenafil dosing up to 80 mg three times daily is safe and well tolerated from an ocular perspective in patients with pulmonary arterial hypertension, and that daily chronic dosing in this patient population was not associated with visual change and had no detrimental effect on best corrected visual acuity, contrast sensitivity, color vision, or visual field, or on slit lamp examinations, funduscopy, or intraocular pressure during the duration of this study.

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



FDA Acts to Bolster Supply of Critically Needed Cancer Drugs



The FDA announced a series of steps to increase the supply of critically needed cancer drugs.


In response to the critical shortage of the cancer drug Doxil (doxorubicin hydrochloride liposome injection) and rapidly declining supplies of methotrexate, the FDA took proactive steps needed to increase available supply for patients in the U.S. For Doxil, there will be temporary importation of a replacement drug, Lipodox (doxorubicin hydrochloride liposome injection), which is expected to end the shortage and fully meet patient needs in the coming weeks. For methotrexate, in addition to already announced actions, the Agency has approved a new manufacturer of preservative-free formulation of methotrexate that is expected to further bolster supply and help avert a shortage of this lifesaving medicine.  FDA expedited review of the application to help address this potential shortage.


In addition, FDA today issued draft guidance to industry on detailed requirements for both mandatory and voluntary notifications to the agency of issues that could result in a drug shortage or supply disruption. Under FDA’s exercise of enforcement discretion the chemotherapeutic drug Lipodox will be imported as an alternative to Doxil. Doxil is used in multiple treatment regimens, including treatment of ovarian cancer after failure of platinum-based chemotherapy. The drug is also indicated for use in AIDS-related Kaposi’s sarcoma and multiple myeloma. FDA anticipates that the incoming supply of Lipodox will be able to fully meet patient needs. FDA’s exercise of enforcement discretion for Lipodox is a temporary, limited arrangement specific to Sun Pharma Global FZE and its authorized distributor, Caraco Pharmaceutical Laboratories Ltd.


Temporary importation of unapproved foreign drugs is considered in rare cases when there is a shortage of an approved drug that is critical to patients and the shortage cannot be resolved in a timely fashion with FDA-approved drugs. When a company is identified that is willing and able to import the needed drug product, FDA evaluates the foreign-approved drug to ensure that it is of adequate quality and that the drug does not pose significant risks for US patients. Only after successful evaluation of these factors does FDA exercise its enforcement discretion for the temporary importation of an overseas drug into the U.S. market.


With regard to methotrexate, a drug that is needed for the treatment of many forms of cancer and other serious diseases, FDA has successfully engaged many firms to assist in maintaining supplies to meet all patient needs. Preservative-free methotrexate is needed for the intrathecal (injection into the fluid surrounding the brain and spinal cord) treatment of children with acute lymphocytic leukemia (ALL) and for the high-dose therapy of osteosarcoma.


First, FDA has prioritized review of and approved a preservative-free methotrexate generic drug manufactured by APP Pharmaceuticals and expects that product to become available in March and continue indefinitely. Second, Hospira expedited release of additional supplies, resulting in 31,000 vials of new product – enough for more than one month’s worth of demand – being shipped to hundreds of U.S. hospitals and treatment centers. FDA is actively working with other manufacturers of methotrexate who have also stepped up to increase production in order to meet patient needs, including Mylan and Sandoz Pharmaceuticals.


APP’s application for preservative-free methotrexate is a supplement to its already approved generic drug application that the firm had previously discontinued. When FDA became aware of potential problems with the supply of the drug (due to the largest manufacturer, Bedford/Ben Venue voluntarily closing its plant), the Agency reached out to other firms to see how FDA could assist to meet the shortfall.


Prior to approval of APP’s application and subsequent to Ben Venue’s voluntary shutdown, FDA worked with Ben Venue on release of already manufactured preservative-free methotrexate, following confirmation of its safety. This supply is available already and will provide emergency supplies as the other firms also work to increase production of methotrexate in response to requests by FDA and the public.


The Administration also announced on October 31, 2011, its support for bipartisan legislation that would require all prescription drug shortages to be reported to FDA and would give FDA new authority to enforce these requirements. While additional manufacturing capacity is necessary to fully address the drug shortage problem, additional early notification to FDA can have a significant, positive impact on addressing the incidence and duration of drug shortages.

The Pre-Existing Condition Insurance Plan – Success or Boondoggle?


By Mark L. Horn, MD, MPH, Chief Medical Officer, Target Health Inc.


A progress report from the Center for Consumer Information and Insurance Oversight (CCIIO) on an element of the Affordable Care Act (ACA) was issued this week and seemed to attract less attention than typically accrues to ACA matters. Perhaps some have forgotten, but the ACA created a temporary mechanism for uninsured patients with pre-existing conditions to secure health coverage prior to 2014 when the ACA established Insurance Exchanges, mandating that all insurers cover pre-existing conditions, become operational. The idea is straightforward, there are many Americans who, due to job loss, disability, financial distress or simple bad luck find themselves uninsured, and among this group there is a doubly unfortunate segment that has a pre-existing significant health problem. This combination of events creates a potentially unsolvable and financially ruinous problem, uninsurable health costs.


Since this dilemma, widely known and lamented, was intensively discussed during the health reform debates, it’s surprising that this report has not received more attention. The program, labeled the Pre-Existing Condition Insurance Plan (PCIP) is operational, and will have enrolled nearly 50,000 people in either federally or state run (it is structured on a ‘Federalist’ model) PCIPs through December, 2011.


The demographics of the enrollees suggest that the program has attracted, as presumably was anticipated, individuals who for a variety of reasons are unable to secure employer coverage and are too young for Medicare, a population long recognized as especially vulnerable to the coverage ?cracks’ in our health system. Among medical needs covered, and specifically cited in the report, are cancer, circulatory disorders, and rehabilitative care including “certain forms of radiation and chemotherapy“. Among criticisms: the current anticipated cost of coverage, nearly $29,000 per member/per year, is significantly higher than the $13,000 estimated in November 2010. The report notes that this reflects the significant and severe medical needs of this especially vulnerable population.


What are we to make of this?


To this observer, it is hard to call this anything but a success. A highly vulnerable population without viable insurance options has been defined, and a mechanism of insuring them at rational premiums (e.g. prices they can manage) has been devised. There is no suggestion in the report that the cost overruns emanate from anything other than legitimate medical expenses; finally, coverage, while ‘actuarially’ subsidized is not free, e.g. premiums are charged and paid.


This seems a particularly American solution, effective, pragmatic, (and imperfect), to a serious social problem affecting a clearly vulnerable group of people. Its imperfections are non-trivial, among these its expense; nevertheless for many it apparently successfully addresses a critical problem. As citizens, we should be proud of, and grateful for, this success.

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

©2012 Target Health Inc. All rights reserved

Cancer Breath Test Enters Clinical Trials


Breath tester: Inside Metabolomx’s device, breath is pumped over arrays of 120 chemical reactants that change color in response to volatile breath biomarkers.
Technology Review



A startup says its test can distinguish between subtypes of lung cancer.



MIT Technology Review, by Katherine Bourzac, February 23, 2012  —  Someday soon a breath test could do more than just tell if you’ve been drinking. Metabolomx, a startup in Mountain View, California, recently completed a clinical trial that shows that its breath test can spot lung cancer with 83 percent accuracy and can also distinguish between several different types of the disease, something that usually requires a biopsy. The accuracy of the test matches what’s possible with low-dose computerized tomography imaging of the lungs.

Existing tests for lung cancer—the leading cause of cancer death worldwide—cause too many false positives, which means patients face unnecessary biopsies or exposure to radiation from imaging, and none are currently approved by Medicare. A breath test promises much simpler, safer screening.

Chemical results of a tumor’s metabolism are dissolved in the blood, and can end up in the breath. Trained dogs can identify breath samples from patients with lung cancer with 98 percent accuracy. Researchers have been working on a noninvasive cancer breath test for years, but have struggled to make one that is simple, reliable, and portable enough. A method called gas chromotography-mass spectrometry can detect metabolites in the breath, but it can’t be done at the bedside, and requires some expertise to operate.

Paul Rhodes, the founder and CEO of Metabolomx, says the company is now running additional lung and colon cancer clinical trials of equipment that is 1,000 times more sensitive to biomarkers carried on the breath than the one used in its recently completed clinical trial. That could help them get to 90 percent accuracy, which Rhodes believes will be necessary to get the test to market.


Breath tester: An engineer at Metabolomx breathes into a breath-analysis machine. Credit:Technology Review



Peter Mazzone, a pulmonologist at the Cleveland Clinic, who is running clinical trials of the new system, says a noninvasive metabolic breath test could help doctors make a better decision when a CT scan looks suspicious. Today, when doctors find a nodule in a patient’s scan, they have to follow up periodically to see if the nodule gets bigger, and then do a biopsy. And eventually Mazzone hopes a metabolic breath test could help predict the behavior of a particular cancer and what drugs it will respond to: “How aggressive is it? Do we need to simply remove it, or remove it and give chemotherapy?”

In the current version of the system, a patient must breathe through a tube for about five minutes. Pumps draw the breath through a series of filters to dry it out and remove bacteria, then over an array of sensors. Metabolomx has shown that the system can distinguish breath samples from patients with different subtypes of lung cancer.

The sensor array consists of colored reactants that are each sensitive to a different group of volatile compounds. Depending on what’s in the sample, different spots in the array—24 in the version used for the initial clinical trial, 130 in the current one—will change color to varying degrees. The system takes a photo of the array of colored reactants before and after they’re exposed to the breath sample, subtracts one image from the other, and generates a colored pattern for that sample.

Rhodes expects a test to cost $75. Also, because it’s not specific to a particular group of chemicals, the Metabolomx sensor could, in theory at least, be used to screen for any disease that has a metabolic breath signature—the company is currently exploring tests for other diseases, including tuberculosis. “A breath signature could give a snapshot of overall health,” Rhodes says.

Next Page →