UMKC School of Pharmacy Update

January 9, 2012 By Leave a Comment

By RUSSELL B. MELCHERT, Ph.D | Dean | UMKC School of Pharmacy

Thank you for the opportunity to update you on the UMKC School of Pharmacy! We are undergoing many changes right now, and this is a very exciting time for us!

Our curriculum has undergone some major changes recently. We have modified our curriculum from a “1-5” to a “2-4.5” meaning that approximately two years of pharmacy prerequisite courses are required for admission to our program, and the professional doctor of pharmacy program is approximately four and one-half years in duration. Functionally, this amounts to moving the “old” first year of our curriculum to prerequisite courses, but most of the courses taken will be the same as before (e.g. general chemistry through organic chemistry). The change required us to go through one year where we do not admit any students. Not having an incoming class this year is somewhat traumatic for most of us on faculty and staff at UMKC, but we will get through it. The worst part for us was telling some great students that they could not apply for admission in 2011. We really look forward to our incoming class next year, and we are already accepting applications for entry in the fall of 2012. All applicants will need to apply through the national PharmCAS system—information on the process is available on our website.

A second major change is that back in June of this year Governor Nixon signed legislation that will provide the funding necessary for us to expand our pharmacy program to the Missouri State University (MSU) campus in Springfield. Even though the economy has exerted a significant negative impact, demand for pharmacists continues to outstrip supply throughout the country, particularly in rural states. Missouri is no exception to this phenomenon, and according to the latest Pharmacy Manpower Project data, Missouri’s demand for pharmacists continues to exceed supply and continues to be higher than the national average. Further, our school of pharmacy continues to receive requests for pharmacists from pharmacies in rural parts of the state. Our expansion of the program to the MU campus in Columbia has helped with this issue to some degree with the vast majority of our first two graduating classes (2010, 2011) filling positions throughout central and southern Missouri. Our graduate placement data trend seems to support the conclusion that regional programs can help meet regional demand for pharmacists. If all goes as planned and we receive approval to expand the program from our accrediting body, then we plan to enroll the first group of students on the MSU campus in the fall of 2014. We are very excited about this opportunity, and we are most grateful for the commitment of our partners at MSU and in the hospitals, clinics, and pharmacies throughout Springfield and the surrounding communities!

Yet another major change is that our enrollment for the fall of 2012 will return to our “pre-Caring for Missourians” level. That is, with the CFM funds, we were able to increase our enrollment by 15 students per year for three years. Beginning next fall, our entering class will go down by 15 and consist of 95 students in Kansas City and 28 students in Columbia. For the fall of 2014, we are planning on admitting 30 students per year at the MSU site. If approved, all students applying to the UMKC School of Pharmacy in 2014 will be able to indicate their preference for Columbia, Kansas City, or Springfield.

We also received several pieces of other good news over the past year. Despite the difficult economy and tight federal funding, our basic science faculty received eight new federal and foundation research grants, supplements to grants, and patents. New grants and/or patents were awarded to Drs. Hari Bhat, Kun Cheng, Santosh Kumar, Simon Friedman, Ashim Mitra, Mridul Mukherji, and Celestin Youan. Together with the rest of our outstanding scholars and researchers, the UMKC School of Pharmacy will most likely move into the upper 25% of pharmacy schools in terms of extramural research next year!

Once again, we find ourselves in very exciting times for the UMKC School of Pharmacy! Students, staff, and faculty alike are all part of a pivotal point in the 125 year history of our great school, and we are grateful for the support the MPA has provided in our education and patient care missions. Wherever you are, you can always assist us and the profession by talking to children about your profession and recruiting them to pharmacy school—it’s never too early to start recruiting! Thank you everyone!

You are all more than welcome to come visit us any time. Just send me an e-mail and let me know when you are coming. We enjoy showing people around the school in Kansas City and in Columbia!

Have a great fall and holiday season!

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New Oral Anticoagulants v. Warfin

January 6, 2012 By Leave a Comment

By JASON R. PELLETIER | UMKC | Pharm.D. Candidate

Since it first appeared on the market in the early 1950s, warfarin has dominated the oral anticoagulation realm and kept many patients from premature thrombotic events. However, warfarin is also associated with a great number of drug and food interactions, trouble with genomic variations, and a narrow therapeutic window that make routine blood tests mandatory. These tests, along with faithful adherence to diet and drug dose (which may change each day) are not always achievable in some patients, and may result in a failure to maintain a therapeutic INR of 2-3. The blood tests and strict diet may also be considered a nuisance even in highly adherent patients. Fortunately for both groups, there are three new oral anticoagulants on the horizon: Eliquis™ (apixaban), Xarelto® (rivaroxaban), and Pradaxa® (dabigatran). These drugs are heralded as the new anticoagulants of the future that do not require monitoring and while this may be ideal in some patients it is not in others. A deeper comparative look between the new drugs and warfarin is necessary to decide which agent to use on a patient-by-patient basis.

Dabigatran is a direct thrombin inhibitor that inhibits factor IIa and is approved for prevention of stroke and systemic embolism in non-valvular atrial fibrillation. Unlike the other two new oral agents, dabigatran is predominately eliminated unchanged and does not interact with P450 enzymes. Dabigatran is, however, a substrate of the p-glycoprotein enzyme, so other drugs affected by this enzyme may cause increased or decreased plasma levels. Dabigatran is also very poorly protein bound, which means dialysis to remove the agent is reasonably possible in emergency situations. Unfortunately, short of a blood transfusion, there are no other agents currently available to reverse dabigatran.

In the RE-LY trial, two different doses of dabigatran (150mg and 110mg both given twice daily) were compared to warfarin; however the FDA has so far approved 75mg and 150mg. Both doses were shown to be non-inferior to warfarin, and the 150mg dose was superior. The 110mg dose of dabigatran showed significantly fewer rates of bleeding when compared to warfarin and higher dosed dabigatran. This would suggest that the 110mg dose of dabigatran may be associated with roughly the same level of anticoagulation as warfarin but has an even better safety profile. The 150mg dose of dabigatran demonstrated significantly lower rates of hemorrhagic stroke but higher rates of gastrointestinal bleeds when compared to warfarin.

Further analysis of the trial demonstrates that there was a trend for fewer strokes (non-hemorrhagic) in patients with warfarin when compared to 150mg of dabigatran as the quality of INR control improved. There were actually lower rates of major bleeding, major gastrointestinal bleeding, and mortality in the highest quartile (patients who spent the most time in a therapeutic INR of 2-3) of the warfarin population compared to 150mg of dabigatran. Dabigatran became statistically safer than warfarin as the time spent in an INR of 2-3 declined, however. Various lab tests such as activated partial thromboplastin time (aPTT), thrombin time (TT), and ecarin clotting time (ECT) may be elevated at therapeutic doses of dabigatran, however, there are no standards in the literature that define the appropriate therapeutic ranges of these lab tests yet. The current approximations for a reference range in those lab values are taken directly from the results seen in the RE-LY trial.

Rivaroxaban is an inhibitor of factor Xa and is approved for post-operative thromboprophylaxis in patients who have undergone hip or knee replacement surgery at an approved dose of 10mg daily (20mg if on concurrent CYP3A4 inducers). Rivaroxaban is also used off-label for the prevention of stroke and systemic embolism in patients with non-valvular atrial fibrillation. Rivaroxaban is a substrate of both p-glycoprotein and metabolized by CYP3A4 so while it may avoid some of the drug and food interactions with warfarin, it will also have additional interactions with substrates, inhibitors, or inducers of either enzyme.

The ROCKET-AF trial demonstrated a once daily dose of 20mg of rivaroxaban was non-inferior to warfarin and caused fewer major bleeding episodes in the prevention of stroke and systemic embolism in non-valvular atrial fibrillation. However, in the same trial, rivaroxaban was also shown to have been associated with a greater number of clinically relevant non-major bleeding episodes that resulted in either transfusion requirements or hemoglobin drops of 2 g/dL or greater. It may be prudent to take some of the results of this trial with a grain of salt, as the time spent in a therapeutic INR (2-3) for the warfarin patients in this trial was only 57.8%.

Like dabigatran, there is no antidote or reversal agent for rivaroxaban. Major clinical trials have not really addressed laboratory monitoring for rivaroxaban. However, PT changes have been shown to correlate well with rivaroxaban concentrations so this may be used to approximate a patient’s level of anticoagulation even though there is no standard therapeutic level in the literature yet. Lastly, even though it’s dosed once daily, rivaroxaban’s half-life is only 5-13 hours which may create a sub-therapeutic problem much faster (when compared to warfarin) in patients who have trouble with adherence.

Apixaban is also an inhibitor of factor Xa, but does not yet have any FDA approved indication and is consequently not on the market. Like rivaroxaban, apixaban is also a substrate of p-glycoprotein and metabolized by CYP3A4. Lastly, like the rest of the new oral agents, there is no antidote or reversal agent available for apixaban and monitoring is not required. The lack of monitoring may also be considered a downfall in certain situations. Very few of the trials out so far address patients with renal or hepatic insufficiency in great detail for any of the new anticoagulants. Treating these patients without under or overdose may be difficult without standardized monitoring parameters.

A recent trial for the drug in atrial fibrillation, ARISTOTLE, was published in the New England Journal of Medicine on September 15th, 2011. In this trial, participants were given 5mg dosed twice daily of apixaban or warfarin with a target INR of 2-3. Patients in the trial had atrial fibrillation and at least one additional risk factor for stroke. The results of this trial demonstrated that apixaban was superior to warfarin in the prevention of stroke or systemic embolism in patients with atrial fibrillation. The trial also demonstrated a lower risk of major and minor bleeding when compared to warfarin.

Like all new drugs, information regarding interactions, safety and efficacy is constantly coming in for the new oral anticoagulants. To date, these agents do not appear to have any major food interactions like warfarin does. However, a fed state in general may increase maximum plasma concentrations as well as the time to reach those concentrations, but does not appear to affect the elimination half-life of rivaroxaban. The manufacturer further recommends taking only the 20mg dose of rivaroxaban with food.

Cost is also a major concern, especially when a new drug comes on the market. In a cost-effectiveness article published by the American Heart Association in 2010, dabigatran 150mg was estimated to be more cost-effective for stroke and systemic embolism prevention in atrial fibrillation patients as compared to warfarin when the time spent in a therapeutic INR (2-3 with warfarin) was < 57.1%. Warfarin, on the other hand, was more cost effective than dabigatran when the time spent at the therapeutic INR was > 72.6%. The current information from the manufacturer states that an opened bottle must be used within 30 days due to drug degradation from moisture, although the manufacturer is currently evaluating stability at 60 days and beyond. The FDA currently recommends using any opened bottle within 60 days. This impaired stability in the presence of moisture has the potential to increase direct drug costs if stored inappropriately and healthcare costs if unaware patients continue to use a product that has been compromised and are no longer therapeutically anticoagulated.

Information presented at the International Society on Thrombosis and Haemostasis in 2009 evaluated the cost-effectiveness of using rivaroxaban over enoxaparin for post-operative DVT prophylaxis in hip and knee replacement patients. The results of this comparison evaluated four different studies and found that rivaroxaban was more cost-effective than enoxaparin (indirect healthcare costs were included). The studies looked at prophylaxis for 10-35 days and within that time frame rivaroxaban was roughly $100-400 cheaper depending slightly on who administered the enoxaparin.

Due largely to the lack of necessary therapeutic monitoring and food interactions, these drugs may be better choices for certain patients that cannot otherwise maintain an INR of 2-3 on warfarin. The drugs may directly cost more than warfarin at this point in time, but when considering the increased indirect healthcare costs due to stroke or systemic embolism for a poor warfarin candidate the new anticoagulants may come out ahead. However, if the only reason a specific patient is unable to maintain a therapeutic INR is due to trouble with adherence to a daily dose of warfarin then dabigatran and abixaban may not immediately counter the problem as they are dosed twice daily. Rivaroxaban also has a half-life significantly shorter than warfarin so intermittent non-adherence will lead to a sub-therapeutic state of anticoagulation and potential thrombotic event much quicker.

While less monitoring may be significantly more convenient for some patients and practitioners alike, it also means the drugs may be more dangerous to use in patient populations that are not as well studied yet, such as those with more severe renal or hepatic insufficiency or patients that are extremely over or under weight. Drug-drug interactions may also become problematic, as some can increase or decrease plasma levels of the anticoagulants and leave a patient sub- or supra-therapeutic for longer periods of time that regular warfarin monitoring would have caught. The risks of exposure to sub- or supra-therapeutic doses carry serious consequences that can lead to death and irreversible bleeding. The inability to reverse any of the three new agents without blood transfusions may also pose additional complications and unforeseen increases in healthcare expenditures when compared to patients that may have been kept out of the hospital if monitored and kept at a therapeutic dose of warfarin or given vitamin K to help reverse a supra-therapeutic warfarin bleed risk.

In summary, while these new agents may be great anticoagulation tools for some patients, they also carry with them potential problems. In general, patients who are poor warfarin candidates and do not spend sufficient time at the therapeutic INR range of 2-3 due to food or drug interactions or possibly adherence (to regular monitoring or different dose adjustments) and have healthy renal and hepatic function are the ideal candidates for the new oral anticoagulants. On the other hand, patients who are able to maintain a therapeutic INR without major complications may find that the new oral anticoagulants are not quite as safe and cost-effective as simply remaining on warfarin at this point in time. As with any new drug, some of this information may change as more and more data from post-marketing studies continues to come in.

References

Shah, Shimoli, MD and Brian Gage, MD, MSc. “Cost-Effectiveness of Dabigatran for Stroke Prophylaxis in Atrial Fibrillation.” American Heart Association. 123. (2011): 2562-2570. Web. 29 Sep. 2011.

Kwong, Louis, Aurea Duran, Alexi Diamantopoulos, Nishan Sengupta and Michael Lees. “Cost-Effectiveness of Rivaroxaban for Prevention of Deep Vein Thrombosis and Pulmonary Embolism after Total Hip or Knee Replacement in US Patients.” International Society on Thrombosis and Haemostasis (ISTH) XXII Congress. Bayer Schering Pharma AG and Johnson & Johnson Pharmaceutical Research & Development, L.L.C. Boston, MA. 11-16 July 2009. Poster Presentation.

Granger, Christopher, et al. “Apixaban versus Warfarin in Patients with Atrial Fibrillation.” New England Journal of Medicine. 365.11 (2011): 981-992. Web. 29 Sep. 2011.

Connolly, Stuart, et al. “Dabigatran versus Warfarin in Patients with Atrial Fibrillation.” New England Journal of Medicine. 361.12 (2009): 1139-1151. Web. 29 Sep. 2011.

Patel, Manesh, et al. “Rivaroxaban versus Warfarin in Nonvalvular Atrial Fibrillation.” New England Journal of Medicine. 365.10 (2011): 883-891. Web. 29 Sep. 2011.

Dabigatran. Lexicomp Online. http://www.lexicomponline.com/. Updated 9/22/11. Accessed 9/29/11.

Rivaroxaban. Lexicomp Online. http://www.lexicomponline.com/. Updated 9/22/11. Accessed 9/29/11.

Dabigatran. Micromedex 2.0. http://www.thomsonhc.com/micromedex2/librarian/. Accessed 9/29/11.

Rivaroxaban. Micromedex 2.0. http://www.thomsonhc.com/micromedex2/librarian/. Accessed 9/29/11.

Apixaban. Micromedex 2.0. http://www.thomsonhc.com/micromedex2/librarian/. Accessed 9/29/11.

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Cystic Fibrosis, Therapies in Pipeline

January 4, 2012 By Leave a Comment

By KAITE A. O’DELL | UMKC | Pharm.D. Candidate

Cystic fibrosis is an autosomal recessive disorder that is the most common deadly genetic disorder found in Caucasians. It affects 70,000 people worldwide with 30,000 being in the United States (1). In 1949, Lowe et al. proposed that cystic fibrosis must be caused by a defect in a single gene due to the autosomal recessive pattern of the inheritance of the disease.

In 1986, Quinton found that sweat ducts in patients with cystic fibrosis are impermeable to chloride. This led to the hypothesis that a defective chloride channel found in the lungs accounted for the respiratory failure and other clinical manifestations of cystic fibrosis. Later in 1989, the gene was identified and named the cystic fibrosis transmembrane conductance regulator (CFTR) (2).

The CFTR protein is responsible for conducting chloride across the cell membrane. It is found in the lungs, pancreas, gastrointestinal tract, sweat glands, liver, and reproductive tract. Mutations in the CFTR gene cause patients with cystic fibrosis to have defective or missing CFTR proteins at their cell surfaces, and results in poor chloride ion and water flow across cell membranes. This causes the body to produce abnormally thick and sticky mucus that leads to chronic life threatening lung infections. The thick mucus disrupts mucociliary clearance, causes neutrophil dominant inflammation, and bacterial colonization resulting in chronic infection. The clinical course of cystic fibrosis is one of episodic exacerbations of pulmonary infection and inflammation interspersed with periods of relative stability (1).

Approximately 4 percent of all Caucasians carry a single CFTR mutation. When 2 mutations are present the CFTR protein does not function. There are 6 different types of mutations of the CFTR protein. Class 1 mutations are caused by premature termination of mRNA translation and result in truncated, nonfunctional CFTR protein. This mutation occurs in around 10 percent of all cystic fibrosis cases. A class 2 mutation is caused by CFTR that is misfolded and then degraded before reaching the apical surface of the cell membrane. The delta F508 mutation is a class 2 mutation and it is the most common mutation found in cystic fibrosis occurs in more than 90% of all patients with cystic fibrosis in the United States. The third class of mutation happens when the channel is unable to use ATP to speed chloride ion transport. The G551D mutation is a class 3 mutation and occurs in 4 to 5% of patients with cystic fibrosis. Mutations of these first three classes have more severe disease manifestations (1).

Until now, medications for cystic fibrosis have not targeted the underlying cause of the disease. Existing medications used for cystic fibrosis include those that increase the airway surface liquid such as inhaled hypertonic saline, anti-inflammatory medications such as steroids and NSayss, antioxidants such as N-acetylcysteine, and inhaled antibiotics such as tobramycin and colistimethate (1). Implementation of these therapies have improved the quality of life of cystic fibrosis patients and increased the median survival age from 11 to 37 years over the past 40 years. However, these therapies only treat the symptoms of cystic fibrosis (3).

Among the new investigational drugs, ivacaftor (Kalydeco or VX-770) is the first medication for cystic fibrosis to work on the CFTR protein that causes the disease. It works by augmenting the chloride-transport activity allowing for an increase in time that the activated CFTR channels at the cell surface remain open in patients with the G551D mutation (4). The maker of ivacaftor, Vertex Pharmaceuticals submitted a new drug application in October of 2011 with a request for Priority Review.

A phase 2 trial (5) by Accurso et al., tested the safety and efficacy of ivacaftor in a 2 phase trial comparing ivacaftor to placebo after 14 days and then after 28 day of treatment. Ivacaftor was found to cause an improvement in lung function after 14 and 28 day treatment regimens compared to placebo. The mean relative change from baseline in the percentage of predicted FEV1 was 10.5% for ivacaftor 150mg every 12 hours after 14 days and 8.7% after 28 days. The frequency of adverse events was similar between the groups.

STRIVE is a phase 3 trial (4) completed by Ramsey et al. and published in the New England Journal of Medicine found that ivacaftor was associated with an improvement in lung function at 2 weeks that remained throughout the 48 week study. The percent predicted FEV1 was increased by 10.6% in the ivacaftor group compared to the placebo group after 24 weeks. Other improvements were also seen in the risk of pulmonary exacerbations, patient-reported respiratory symptoms, weight, and concentration of sweat chloride. Patients receiving ivacaftor were 55% less likely to have a pulmonary exacerbation than placebo over the 48 weeks. Subjects in the ivacaftor group scored 8.6 points higher than did subjects in the placebo group on the respiratory-symptoms domain of the Cystic Fibrosis Questionnaire. By 48 weeks, subjects had also gained an average of 2.7 kg more weight than the placebo group. The concentration of sweat chloride was -48.1 mmol per liter with ivacaftor compared to placebo at 48 weeks. The incidence of adverse events was similar with between groups with a lower proportion of serious adverse events with ivacaftor.

ENVISION is another phase 3 trial that studied the use of ivacaftor in children ages 6-11 years. A press release by Vertex Pharmaceuticals state that children who received ivacaftor experienced rapid and sustained improvements in lung function, weight gain, and reduction of sweat chloride throughout 48 weeks. The mean absolute improvement in lung function for children treated with ivacaftor was 10% compared to placebo and a relative mean improvement was 15.1% from baseline compared to placebo. Adverse effects were comparable between treatment groups(6).

PERSIST is a phase 3, open-label 96 week extension study of both the ENVISION and STRIVE trials. Vertex Pharmaceuticals released data from the first 12 weeks of the study in a press release. They found that the improvement in lung function was sustained through week 12 of the study for a total of 60 weeks of treatment. Adverse events were similar to those observed in the STRIVE trial (6).

Ivacaftor also stimulates activity in the delta F508-CFTR, the most common mutation in cystic fibrosis patients. However, it is much less active on the delta F508 than the G551D CFTR gene and clinical benefit in these patients is unknown. It is also not yet evident as to whether ivacaftor will stop the progression of deterioration in lung function in patients with cystic fibrosis (3).

There are other drugs being developed currently for cystic fibrosis as well. A promising candidate is the combination of VX-770 (ivacaftor) and VX-809 which will be used to treat patients with the most common mutation, the delta F508 mutation (1). The combination drug is currently in a phase 2 trial, in which Vertex Pharmaceuticals released a statement that at 28 days the combination was well tolerated and had a statistically significant change in sweat chloride suggesting increased CFTR activity (7). The findings of these studies represent an important milestone in the development of treatments designed to tackle the underlying cause of cystic fibrosis.

References:

1. Anderson P. Emerging Therapies in Cystic Fibrosis. Ther Adv Resp Dis. 2010; 4: 177-185.

2. Rowe SM, Miller S, Sorscher EJ. Cystic Fibrosis. N Engl J Med 2005; 352: 1992-2001.

3. Davis PB. Therapy for Cystic Fibrosis – The End of the Beginning? N Engl J Med 2011; 365: 1734-1735.

4. Ramsey BW, Davies J, McElvaney G, et al. A CFTR Potentiator in Patients with Cystic Fibrosis and the G551D Mutation. N Engl J Med 2011; 365: 1663-1672.

5. Accurso FJ, Rowe SM, Clancy JP, et al. Effect of VX-770 in Persons with Cystic Fibrosis and the G5512-CFTR Mutation. N Engl J Med 2010; 363: 1991-2003.

6. Partridge M, Pike , Osborne M. Phase 3 Study of KALYDECO (ivacaftor) in Children Ages 6-11 with a Specific Type of Cystic Fibrosis Showed Significant Improvements in Lung Function and Other Measures of Disease Sustained Through 48 Weeks. Vertex Pharmaceuticals Incorporated. November 3, 2011. Retrieved Nov 14, 2011 from http://investors.vrtx.com/releasedetail.cfm?releaseid620643.

7. Patridge M, Pike L, Osborne M et al. Interim Phase 2 Data Showed a Combination of VX-770 and VX-809 Improved Function of the Defective Protein that Causes Cystic Fibrosis in People With the Most Common Form of the Disease. Vertex Pharmaceuticals Incorporated. June 9, 2011. Retrieved Nov 14, 2011 from: http://investors.vrtx.com/releasedetail.cfm?releaseid=583683.

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Member profile: Scott Cady, Pharm.D.

January 2, 2012 By Leave a Comment

By JOHN SPRINGLI | Communications Manager | MPA

Situated in the middle of downtown in the quaint northwest Missouri town of Chillicothe is Hometown HealthMart Pharmacy, home to Scott Cady. Working side-by-side with his wife Mary, he is one of the lead pharmacists at Hometown as well as a partial owner. To top it all off, as pharmacy technician Jessica Zeger says, “he’s the best boss I’ve ever had to work with.”

Scott has been working at Hometown since 2006 when he graduated from the University of Kansas with a Doctor of Pharmacy degree. This, however, was not his start into the world of pharmacy.

Growing up in the Kansas City area, his father worked in the pharmaceutical industry doing research and development and Scott planned on going along similar lines as he attended Baylor University. After graduation, he moved north to Cincinnati, Ohio to work for a pharmaceutical research company but ultimately knew he needed to continue his education. Eventually, Scott moved back to the Kansas City area and enrolled at the KU School of Pharmacy in 2002. While in school, Scott says his areas of interest shifted from research based to more clinically thinking.

Scott moved to Chillicothe in 2006 and began working at Hometown, where he met Melissa King. While the two are similar in age, she was a veteran to him since she had been in the business for near six years before he came to Hometown. She says it was interesting working with him at the beginning because while he was clinically based, he still brought on that research side he had learned in Ohio and prior. This way of thinking varied from her own real-world practical setting ideal.

“He really looks at all the clinical aspects and evaluates the patient and the medication,” King says. It’s nice that we all think a little differently and bring different aspects to the table for the same result.

Being there for the patients is another strong asset that Scott brings to the table according to King.

“I would put him up with any doctor on his bedside manner,” she says.

Keeping his patients in mind is something Zeger says he does an “A+ job at.” Several days prior, Zeger says, an elderly patient whose son had just passed away suddenly came into Hometown and ended up breaking down and crying in Scott’s arms and before the staff knew it, Scott was tearing up right along side the patient.

“You wouldn’t see that in another pharmacy,” Zeger says. “We all know these people by name as soon as they walk in the door and I think that is the most important thing.”

In the fall of 2006 Scott joined the Missouri Pharmacy Association. One of his first duties was being apart of the Continuing Education committee, followed by the new membership committee and finally to his current post as a Member-at-Large of the Board of Directors. While he has worn several different hats for the MPA, he says he’s always known joining was the best thing to do.

“While I was at the University of Kansas, I was greatly involved with the Kansas Pharmacy Association as well as the American Pharmacist Association, so being in associations and being able to help direct our profession or educate the people who help direct our profession has kind of always been there for me. Joining MPA was kind of a no brainer,” says Scott. “I want to make sure we do what we want to do that’s in the best interest of our patients.”

While he may be a Jayhawk in Tiger country, he is still a dedicated pharmacist to all his patients and staff, he is also a wonderful husband and father to his wife and two small children say King and Zeger. Scott and his wife Mary have a 2-year-old son who in Scotts words, “will be more intelligent than he is some day,” and a 3-month-old daughter who was born over the summer.

“I’ve seen Scott and his wife Mary as they went from newlyweds to growing their family,” King says. “They’re learning how to balance pharmacy with being parents and the fact that Scott’s still devoted to organizations like MPA shows that they know what life’s all about.”

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Pharmacists Mutual Announces Edward J. Yorty as New President

December 30, 2011 By Leave a Comment

By LAURIE HARMS | Pharmacists Mutual Companies

Pharmacists Mutual Insurance Company Board of Directors has named Edward J. Yorty to serve as the company’s President. Yorty was also elected Director to the Pharmacists Mutual Insurance Company and The Pharmacists Life Insurance Company Boards.

Ed Yorty has over 20 years of experience in the insurance industry, including the last 15 years working for mutual insurance companies. Most recently, he served as CFO of Oregon Mutual Insurance and prior to that, he served the physicians and dentists of Maryland, Pennsylvania, Virginia, and Washington D.C. as Vice President and Actuary at Medical Mutual Liability Insurance Society of Maryland.

Yorty is a Fellow of the Casualty Actuarial Society and a member of the American Academy of Actuaries. He has a Bachelor of Science Degree in Meteorology from Pennsylvania State University, and he is currently enrolled in Northeastern University’s Master of Finance Program.

Chief Executive Officer, Ed Berg, stated, “The Pharmacists Mutual Board of Directors conducted a nationwide search for my successor, and we are very pleased to find someone with Ed Yorty’s experience and credentials. We believe he will continue our company’s legacy of forward thinking operations coupled with the highest level of emphasis on customer service and value. In addition, Ed will be visible and active in the pharmacy community as well as in our home office community of Algona, Iowa.”

Ed and his wife, Tammy, have settled into Algona with their three dogs. When Ed is not working, he enjoys running with his dogs and has run Oregon’s 200 mile Hood to Coast Relay six times. He also enjoys skiing, reading and learning German.

Ed Berg will continue as Pharmacists Mutual Companies CEO until spring 2012 when Ed Yorty will succeed him as President and CEO.

Pharmacists Mutual Companies are licensed in 49 states and the District of Columbia, and serve over 70,000 customers. Pharmacists Mutual Companies provide business, personal, life, health, and investment products for its core markets of pharmacy, home medical/home health, and card & gift stores. Learn more at www.phmic.com or call 800.247.5930. or 573.519.4551

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