ClinPharm ClinPharm ClinPharm DOM Schulich UWO
Patient Care


Personalized Medicine
Richard B. Kim MD, FRCPC
Professor of Medicine, Physiology & Pharmacology, and Oncology
Clinic phone number: 519-685-8500 ext 34340
Fax: 519-663-3090
Referrals must be from a physician (for inquiries and referral forms, call the number noted above or email: Julie.Mayo@Lhsc.on.ca).

In my personalized medicine clinic located at the London Health Sciences Centre (LHSC)-University Hospital (339 Windermere Road, London, Ontario, Canada), we assess patients on certain medications where genetic variation in their ability to breakdown (metabolize) or respond to drugs may be a reason for lack of drug efficacy or adverse drug response. When appropriate, we measure drug and drug metabolite levels using a latest generation liquid chromatography-tandem mass spectrometry (LC-MS/MS) system. My clinic does not assess patients who have allergic drug reactions. My expertise is in pharmacogenomics and clinical pharmacology where emerging research insights are utilized to deliver personalized medicine-based care to our patients. Currently, I see patients in relation to drugs noted below.
  • Personalized Warfarin Clinic: Since opening in September 2008, we have seen over 700 patients and actively following over 200 patients on the blood thinning drug, warfarin (CoumadinTM) for the treatment of atrial fibrillation. When appropriate, we will test for genetic variation in two genes, CYP2C9 and VKORC1 for determining optimal starting dose of warfarin. Several physicians, including myself, are a part of this clinic.

  • Personalized Statin Therapy: 10-15% of patients on a statin (cholesterol lowering drugs such as atorvastatin (LipitorTM), simvastatin (ZocorTM), and rosuvastatin (CrestorTM), complain of muscle aches and weakness. In the vast majority of such patients, such symptoms do not lead to worsening of symptoms or result in actual muscle injury. However, in a small subset of such patients, recent data clearly show that patients who possess a commonly occurring genetic variation in a drug transporting protein called OATP1B1 (gene name SLCO1B1 (formerly known as OATP2 and OATP-C) that my group discovered in 2001, have a nearly 18-fold greater risk for statin-induced myopathy (muscle injury)). In this clinic, after the patient is assessed, a detailed report and recommendation to the referring physician are provided regarding SLCO1B1 genotype, statin level (when relevant), and recommended statin dosing or switching.

  • Personalized Tamoxifen Therapy: I started this clinic at the London Health Sciences Centre-University Hospital in March 2010. We believe this is the first clinic of its type in Canada to provide a real world referral/consultation support for patients at risk for suboptimal tamoxifen therapy for breast cancer. This is important in that breast cancer patients are prescribed a single dose of this medication (20 mg/day) and typically for 5 years. We carry out genotyping for CYP2D6 and also measure blood level of tamoxifen and its active metabolite endoxifen. I have assessed well over 300 patients receiving tamoxifen in this clinic so far, and provide guidance to referring oncologists regarding those patients at risk for suboptimal tamoxifen therapy.

  • Personalized Antiplatelet Therapy: Clopidogrel (Plavix) is an important drug used to prevent the formation of certain types of unwanted blood clots by reducing the stickiness of platelets. Clopidogrel is prescribed to some patients who have had a recent heart attack, stroke, or after insertion of a stent in large blood vessels in the heart called coronary arteries. Clopidogrel is inactive. In the liver, clopidogrel is converted to the active form of the drug called H4 by a drug metabolizing enzyme called CYP2C19. Commonly occurring genetic differences in CYP2C19 can affect its activity and ability to break-down drugs such as clopidogrel. Patients with normal CYP2C19 activity can readily break-down clopidogrel to the active drug (H4). In my clinic, genotyping for CYP2C19 can be carried out to identify those who may benefit from clopidogrel (those who do not have CYP2C19 loss of function genetic variations) as well as those who might be better suited for other antiplatelet drugs (such as ticagrelor or prasugrel) if they carry loss of function CYP2C19 polymorphisms. In addition, when warranted, we can measure the blood level of clopidogrel active metabolite (H4).