Our genes not only determine
our traits but also influence
how medications affect us.
We provide our service for patients who are obliged to take medication frequently and long term, as well as for people for whom a treatment failure or an intolerance can have severe consequences. SONOGEN XP is also suitable for patients who do not tolerate their current treatment.
Our service may also be of interest for anyone who wants to analyze his or her pharmacogenetic profile and thus wants to be prepared in case of a medical treatment. The patient would then receive from the very beginning the most suitable medicine with the optimal dose.
Every person is unique. That is particularly true in the field of medicine.
What cures one person can be either entirely ineffective or cause serious side effects in another.
This problem is not an isolated incidence – on the contrary: In the case of antidepressants, asthma medications and oral antidiabetic drugs, only some 60 percent of patients respond to these therapies. And these are only a few examples. For Alzheimer’s treatments, it is only 30 percent. The source of these statistics lies in factors including our genetic makeup. Among patients taking the same medications, genetic differences can account for differences in factors such as the systemic concentration of an active ingredient. That happens because the active ingredient is absorbed, distributed, or broken down by everyone’s body differently. SONOGEN XP specializes in personalized medicine: Our vision is to identify a customized therapy for every patient in advance.
Our genes are not just the source of these differences in the way drugs work: They also provide the key to successful therapies. Pharmacogenetics (PGx) is the study of how an individual’s genetic makeup affects drug efficacy. It involves identifying variable sequences in the genome, which allows us to determine patients for whom certain medications are ineffective or who have a heightened risk of undesirable side effects. Our SONOGEN XP PGx expert system draws on a pharmacogenetic database with scientific decision-making algorithms. Using the genotyping results, patient information and the prescribed drug, we develop a customized therapy matching each patient’s individual profile.
A 64-year-old patient was treated with oxycodone and diclofenac for chronic pain. Oxycodone is an opioid analgesic which is converted by the enzyme CYP2D6 into an active metabolite, which is 14 times more potent. The pharmacogenetic profile (PGx) developed for the patient showed a genotype/phenotype that lacks CYP2D6 enzyme activity (poor metabolizer, PM), which means that the drug cannot be converted to the more potent active metabolite. This was probably the reason for inadequate pain relief. Therefore, the patient was switched to tapentadol. The therapeutic goal of pain relief was achieved by the second week following this transition and was assured for the long term.
In a female patient, it had proved difficult to adjust oral anticoagulation with a warfarin-type drug. The question was whether this problem resulted from or was influenced by a genetic cause. The personal pharmacogenetic profile (PGx profile) revealed a genotype/phenotype associated with increased sensitivity to warfarin-type drugs. The patient had a variant with reduced enzyme activity for both VKORC1 and CYP2C9. Patients with this constellation require a lower dose of the anticoagulant, which is difficult to regulate, often resulting in phases of excessive and inadequate dosing, both of which may prove dangerous for the patient. With inadequate dosage, the treatment is ineffective, resulting in an increased tendency to form thrombi ("blood clots"), while excessive dosage results in an increased tendency for bleeding.
After testing, the patient was switched to a relatively new group of directly acting oral anticoagulants. Here, too, the PGx profile proved very useful, since this patient also showed a large number of variants for other pharmacologically active genes. Rivaroxaban was thus excluded (one member of the relatively new class of alternative anticoagulants mentioned above), because it is metabolized by the enzyme CYP3A4. The patient's individual PGx profile had also shown reduced activity for this enzyme. This meant that there was a risk of excessive drug effect if one prescribed rivaroxaban. The patient was switched to dabigatran. By selecting this medication, it was possible to achieve the aim of therapy while eliminating the potential adverse effects and risks as described above.