Complex genetic & medication information shouldn’t be hard to use.
Comprehensive Panel
EffectiveRX helps you create a holistic treatment plan based on your patient's genetics and best in class medication management tools
Call us at (866) 932-0109
Discover how EffectiveRX can assist you in getting your patients on the best medication(s) for them
Complex genetic & medication information shouldn’t be hard to use.
Comprehensive Panel
EffectiveRX helps you create a holistic treatment plan based on your patient's genetics and best in class medication management tools
Call us at (866) 932-0109
Discover how EffectiveRX can assist you in getting your patients on the best medication(s) for them
Complex genetic & medication information shouldn’t be hard to use
Our Medication Action Plan (MAP) combines appropriateness tools, PharmD expertise and genetic results to provide a clear, concise patient-centric MAP for treatment, including:
- Established Explicit Medication tools, including BEERs, Anticholinergic Burden, FDA Black Box Warnings, and more
- Published clinical and scientific data
- Genetic Results
- Lifestyle Factors
- Medication History & Potential Medications, including over-the-counter medications
- PharmD Expertise
The Pharmacogenomics Appraisal, Evidence Scoring and Interpretation System (PhAESIS) combines this information to create a holistic treatment plan. This is translated into EffectiveRX’s MAP Report.2
Personalized Medicine
No two people are alike.
Nor is their response to medication.
Do you have patients who are taking multiple medications and are struggling?
Polypharmacy increases the risk of adverse drug reactions caused by a patient’s genetics.1
The Impact of
Polypharmacy
Due to comorbidities in an aging population, polypharmacy is a prevalent challenge in long-term care facilities.3 Polypharmacy often results from comorbidities and has many other negative impacts, including:
PATIENTS
- Decreased Quality of Life
- Increased mobility issues
- Increased mortality
- Increased risk of disability, falls, frailty, inappropriate medication use, long-term care placement & Medication nonadherence 1
Providers
- Decreased physician functionality (workflow impairment, decreased quality of care)
- Decreased physician productivity
- Increased burden on the health care system
- Increased medication errors 1
Common reasons for prescribing
History of Medication Failures
Experienced adverse drug reaction or sensitivity to prescribed medication(s)
Medication Class is new to the patient
Desired medication for the patient has FDA warnings
An “Inhibitor” or “Inducer” may affect therapeutic response to prescribed medication
A component of medical decision making for which medication(s) to avoid, prescribe or titrate
Are your patients experiencing diminished efficacy and/or side effects from these current medications? Or are you considering a new therapy?*
Anticoagulants
Coumadin (warfarin)
Jantoven (warfarin)
Cardiology
Coreg (carvedilol)
Crestor (rosuvastatin)
FloLipid (simvastatin)
Lescol (fluvastatin)
Plavix (clopidogrel)
Rythmol (propafenone)
Zocor (simvastatin)
Dyskinesia
Austedo (deutetrabenazine)
Ingrezza (valbenazine)
Xenazine (tetrabenazine)
Gastroenterology
Antivert (meclizine)
Dexilant (dexlansoprazole)
Marinol (dronabinol)
Prilosec (omeprazole)
Prevacid (lansoprazole)
Protonix (pantoprazole)
Reglan (metoclopramide)
Zofran (ondansetron)
Gaucher's Disease
Cerdelga (eliglustat)
Immunology
Evoxac (cevimeline)
Prograf (tacrolimus)
Protopic (tacrolimus)
Infectious Disease
Reyataz (atazanavir)
Sustiva (efavirenz)
Vfend (voriconazole)
Neurology
Briviact (brivaracetam)
Dilantin (phenytoin)
Onfi (clobazam)
Xenazine (tetrabenazine)
Oncology
Adrucil (fluorouracil)
Balversa (erdafitinib)
Efudex (fluorouracil)
Fluoroplex (fluorouracil)
Iressa (gefitinib)
Pegasys (peginterferon alfa-2a)
Pegintron/Sylatron (peginterferon alfa-2b)
Soltamox (tamoxifen)
Tolak (fluorouracil)
Xeloda (capecitabine)
Pain Management
Ansaid (flurbiprofen)
Celebrex (celecoxib)
Chlortenoxicam (lornoxicam)
Codeine
Feldene (piroxicam)
Hydrocodone
Ibuprofen
Mobic (meloxicam)
Mobiflex (tenoxicam)
Ocufen (flurbiprofen)
Olinvyk (oliceridine)
Ultram (tramadol)
Psychiatry
Abilify (aripiprazole)
Adderall (amphetamine)
Anafranil (clomipramine)
Aristada (aripiprazole lauroxil)
Celexa (citalopram)
Clozaril (clozapine)
Effexor (venlafaxine)
Elavil (amitriptyline)
Fanapt (Iloperidone)
FazaClo (clozapine)
Lexapro (escitalopram)
Luvox (fluvoxamine)
Mellaril (thioridazine)
Norpramin (desipramine)
Orap (pimozide)
Pamelor (nortriptyline)
Paxil (paroxetine)
Rexulti (brexpiprazole)
Silenor (doxepin)
Strattera (atomoxetine)
Surmontil (trimipramine)
Tofranil (imipramine)
Trilafon (perphenazine)
Trintellix (vortioxetine)
Versacloz (clozapine)
Wakix (pitolisant)
Zoloft (sertraline)
Urology
Detrol (tolterodine)
The above medications have actionable gene-drug relationships according to CPIC Levels A&B as well as FDA recommendations.
Many additional medications are also reviewed, reported and categorized based on clinical evidence.
*An EffectiveRX Comprehensive test is intended as an aid to guide medication management decisions for patients who are prescribed to or under consideration for prescription medications associated with but not limited to cardiovascular health, psychiatry, pain management, addiction, or thrombophilia.
Comprehensive Test Panel
| Gene | Gene-Drug Interaction |
|---|---|
| ABCB1(rs1045642) | ABC proteins transport various molecules across extra- and intra-cellular membranes and is a major contributor in the intestinal absorption of ABCB1 substrates. Poor and intermediate ABCB1 phenotypes may have an increased likelihood of therapeutic failure compared to patients with a normal phenotype and taking ABCB1 substrates. Example Substrates: aliskiren, ambrisentan, clopidogrel, colchicine, dabigatran etexilate, digoxin, everolimus, fexofenadine, imatinib, lapatinib, maraviroc, nilotinib, posaconazole, ranolazine, saxagliptin, sirolimus, sitagliptin, talinolol, tolvaptan, topotecan. Ref: 3, 32, 33. |
| ABCG2 | ABCG2 encodes the transporter adenosine triphosphate (ATP)–binding cassette G2and is expressed in many different tissues, including liver, blood-brain barrier, and intestine. ABCG2 facilitates the export of compounds into the extracellular space. This protein protects our cells and tissues against various xenobiotics. Example Substrates: daunorubicin, doxorubicin, rosuvastatin, sulfasalazine, topotecan. Ref: 3, 34. |
| ADRA2A | The Alpha-2-adrenergic receptor is involved in signaling the release of norepinephrine from sympathetic nerves and from adrenergic neurons in the central and peripheral nervous systems. Mental Health: HET/MUT: In clinical studies, patients with the heterozygous or mutant genotype of the adrenergic α2A receptor (ADRA2A) gene may have decreased release of the neurotransmitter norepinephrine in the central nervous system which may lead to decreased response to certain antidepressants: SSRIs (i.e. paroxetine {Paxil}), SNRIs (i.e. milnacipran {Savella}), and ADHD drugs (i.e. methylphenidate {Ritalin}). WT: Patients with the ADRA2A wild-type genotype should expect normal response to certain antidepressant such as SSRIs (i.e. paroxetine), SNRIs (i.e. milnacipran) and ADHD drugs (i.e. methylphenidate). (PharmGKB Best Drug Level Evidence Level 3). Ref: 3,4,5 |
| ANKK1 | ANKK1 gene is linked to dopamine receptor D2 (DRD2) with implications in patient response to certain antipsychotic medications. Shares same allelic DRD2 site (rs1800497). Mental Health: MUT: The mutant gene variant in dopamine D2 receptor (DRD2/TAQA) neurotransmission is associated with increased risk of adverse reactions (i.e. weight gain, metabolic changes) to atypical antipsychotics (i.e. olanzapine {Zyprexa}) drug treatment for schizophrenic or delusional disorders. HET: The heterozygous gene variant in dopamine D2 receptor neurotransmission is associated with a moderate increased risk of adverse reactions (i.e. weight gain, metabolic changes) to atypical antipsychotics (i.e. olanzapine) drug treatment for schizophrenic or delusional disorders. WT: Patients with the dopamine D2 receptor wild-type genotype should expect normal response to atypical antipsychotics (i.e. olanzapine). Mutant/Heterozygote genotypes are associated with improved response to risperidone, aripiprazole compared to patients with the Wild Type genotype. (CPIC Level best drug: C/ PharmGKB Level Best drug: 3) PharmGKB. Web site. Accessed November 1st, 2022. Ref: 3, 6. |
| ApoE | APOE (Apolipoprotein E) gene encodes for the formation of apolipoprotein E which combines with fats (lipids) in the body to form lipoproteins. Lipoproteins are responsible for forming cholesterol and other fats found through the bloodstream. Studies have shown individuals who carry one or more copies of APOE-4 have a reduced therapeutic response to lipid-lowering medications (statins). The APOE-4 allele has shown to have an increased risk of high LDL cholesterol and both cardiovascular disease and Alzheimer’s disease. Ref: 3, 35, 36. |
| COMT | Catechol-O-Methyltransferase (COMT) is an enzyme that inactivates catecholamines, such as epinephrine, norepinephrine and dopamine. COMT regulates cognitive function, memory, mood and pain perception. Mental Health: HET/MUT: Patients with the heterozygous or mutant genotype of the COMT gene may have decreased availability of norepinephrine and dopamine neurotransmitters which may impair the efficacy of certain anti-depressants (i.e. fluoxetine (Prozac), paroxetine (Paxil), other SSRIs, venlafaxine {Effexor}) and lead to reduced response during treatment. WT: Patients with the COMT wild-type genotype should expect normal response to certain antidepressants (i.e. fluoxetine , paroxetine , other SSRIs, venlafaxine ). Pain: MUT: Patients with the COMT Met/Met genotype should expect adequate pain relief with standard doses of opioids (i.e. morphine, fentanyl). HET: In a clinical study evaluating how genes could predict morphine dose for cancer pain relief, patients with the COMT Val/Met genotype required @20% higher morphine doses compared to Met/Met genotype. WT: In a clinical study evaluating how genes could predict morphine dose for cancer pain relief, carriers of the COMT Val/Val genotype required @60% higher morphine doses compared to carriers of Met/Met genotype. Other various gene-drug variant associations include Risperidone, methadone, buprenorphine. (CPIC level best drug: C/PharmGKB best level:3) Ref: 1,2,3, 19, 20, 21 |
| CYP1A2 | CYP1A2 Gene-Drug variant associations affecting drug response/metabolism include caffeine, carbamazepine, clozapine, escitalopram, paroxetine. (PharmGKB Best Drug level:3) PharmGKB Web site. http://Clinical Guideline Annotations (pharmgkb.org). Accessed November 2nd, 2022. |
| CYP2B6 | CYP2B6 Gene-Drug variant associations affecting drug response/metabolism include bupropion, efavirenz, methadone (CPIC Level Best drug: A/PharmGKB Best Drug level: 1A) PharmGKB Web site. http://Clinical Guideline Annotations (pharmgkb.org). Accessed November 2nd, 2022. https://cpicpgx.org/guidelines/cpic-guideline-for-efavirenz-based-on-cyp2b6-genotype/) Accessed November 2nd, 2022. |
| CYP2C8 | This gene encodes for the formation of CYP2C8 enzymes influencing variability in metabolism of approximately 5% of medication. Some examples of CYP2C8 substrates are amiodarone, diclofenac, ibuprofen, montelukast, paclitaxel, pioglitazone, repaglinide, rosiglitazone, tacrolimus, torsemide. (CPIC Level best drug: C/ PharmGKB Level Best drug: 3) )/ Genes-Drugs – CPIC (cpicpgx.org)/ PharmGKB Web site. http://Clinical Guideline Annotations (pharmgkb.org). Accessed November 2nd, 2022. |
| CYP2C9 | CYP2C9 Gene-drug variant associations affecting drug response/metabolism include celecoxib, flurbiprofen, fosphenytoin ,ibuprofen, losartan, meloxicam, phenytoin, warfarin. (CPIC Level best drug: A/ PharmGKB Level Best drug:1A) ) PharmGKB Web site. http://Clinical Guideline Annotations (pharmgkb.org). Accessed November 2nd, 2022.Ref: 37, 38, 39 |
| CYP2C19 | CYP2C19 Gene-drug variant associations affecting drug response/metabolism include amitriptyline, citalopram, clomipramine, clopidogrel, imipramine, lansoprazole, omeprazole, pantoprazole, sertraline, voriconazole. (CPIC Level best drug: A/ PharmGKB Level Best drug:1A) ) PharmGKB Web site. http://Clinical Guideline Annotations (pharmgkb.org). Accessed November 2nd, 2022. Ref: 40-44. |
| CYP2D6 | CYP2D6 Gene-drug variant associations affecting drug response/metabolism include amitriptyline , atomoxetine, codeine , desipramine, doxepin, fluvoxamine, imipramine, metoprolol, nortriptyline, ondansetron, paroxetine ,risperidone, tamoxifen, tramadol, venlafaxine. (CPIC Level best drug: A/ PharmGKB Level Best drug:1A) PharmGKB Web site. http://Clinical Guideline Annotations (pharmgkb.org). Accessed November 2nd, 2022. Ref: 43-48. |
| CYP3A4 | CYP3A4 Gene-drug variant associations affecting drug response/metabolism (ex. exposure, clearance) include atorvastatin, cyclosporine, oxycodone, quetiapine, simvastatin, tacrolimus. (CPIC Level best drug: C/ PharmGKB Level Best drug:1B)/ Genes-Drugs – CPIC (cpicpgx.org)/PharmGKB Web site. http://Clinical Guideline Annotations (pharmgkb.org). Accessed November 2nd, 2022. |
| CYP3A5 | CYP3A5 Gene-drug variant associations affecting tacrolimus drug dosing requirements/metabolism. (CPIC Level best drug: A/ PharmGKB Level Best drug:1A)/ Genes-Drugs – CPIC (cpicpgx.org)/ CPIC: https://cpicpgx.org/guidelines/guideline-for-tacrolimus-and-cyp3a5/) PharmGKB Web site. http://Clinical Guideline Annotations (pharmgkb.org). Accessed November 2nd, 2022. |
DBH(1021C| Dopamine Beta-Hydroxylase (DBH) gene encodes for the formation of dopamine beta-hydroxylase protein. DBH protein catalyzes the hydroxylase of dopamine to norepinephrine and is primarily located in the adrenal medulla and in postganglionic sympathetic neurons. Variations in the DBH gene have been shown to be a risk factor for psychiatric disorders and addiction. Ref: 49, 50, 51 |
|
| DPYD | This gene encodes the dihydropyrimidine dehydrogenase protein, the initial and rate limiting enzyme in the three-step pathway of uracil and thymidine catabolism and the pathway leading to the formation of beta-alanine. The DPYD protein is responsible for degrading fluoropyrimidines, such as 5-fluorouracil, capecitabine, and tegafur. Decreased DPYD activity is associated with a greater than four-fold risk of severe or fatal toxicity from standard doses of 5FU. /) PharmGKB Web site. http://Clinical Guideline Annotations (pharmgkb.org). Accessed March 22nd, 2023. https://cpicpgx.org/guidelines/guideline-for-fluoropyrimidines-and-dpyd/). Accessed March 23rd, 2023. |
| F2 | Patients with the Factor ll gene Prothrombin variant may be at an increased risk of blood clot formation (thrombosis) when exposed to other risk factors such as smoking, pregnancy, obesity, oral contraceptive use, and immobility. The risk is approximately 3-10 times higher in individuals who have one copy of the genetic variant. The risk in people who carry two copies of the genetic variant is unknown. Individuals who do not have a Factor II Prothrombin mutation may still be at increased risk. Other changes in the Factor II gene that were not tested for, changes in other genes, and non-genetic factors may still increase a patient’s risk for thrombosis. PharmGKB Web site. http://Clinical Guideline Annotations (pharmgkb.org). Accessed March 22nd, 2023. Ref: 52, 53 |
| F5 | Individuals with the Factor V Leiden gene variant may be at an increased risk of blood clot formation. This risk is approximately 2-10 times higher in individuals who have one copy of the genetic variant, and greater than 10 times higher for individuals who carry two copies of the genetic variant. Individuals who do not have the Factor V Leiden mutation may still be at increased risk. Other changes in the Factor V gene that were not tested for, changes in other genes, and non-genetic factors may still increase a patient’s risk for thrombosis. PharmGKB Web site. http://Clinical Guideline Annotations (pharmgkb.org). Accessed March 22nd, 2023. Ref: 53, 54 |
| GRIK4 | GRIK4 (glutamate receptor) is the gene that encodes KA1, a type of neurotransmitter receptor subunit that joins together with other subunits to form glutamate receptors. These receptors are located on cells in the brain and are involved in enhancing cell-cell communication, which may play a role in major depressive disorder. This type of receptor primarily binds glutamate, a major neurotransmitter involved in developmental growth, learning and memory. Mental Health: MUT: Patients who are mutant homozygous for the glutamate receptor (GRIK4) gene variant may be more likely to respond to certain SSRI/SNRI antidepressant treatment (i.e. citalopram (Celexa), venlafaxine {Effexor}). WT/HET: Patients with the wild-type or heterozygous genotype of the glutamate receptor may be associated with decreased SSRI/SNRI antidepressant outcome (i.e. citalopram, venlafaxine). (CPIC Level best drug: C/ PharmGKB Level Best drug: 3) Ref: 3, 9, 10 |
| HTR2A (rs7997012) | HTR2A polymorphisms of this serotonin receptor gene may help predict which patients may be more likely to experience SSRI-induced adverse effects and provide information to determine patient response to therapy. Mental Health: MUT/HET: Patients with the mutant or heterozygous genotype of the serotonin 2A receptor gene (HTR2A-1438) should expect to have increased response in improvement of symptoms and /or low risk of adverse side effects when treated with certain SSRIs (i.e. citalopram (Celexa), paroxetine {Paxil}). Improved treatment effect found to be more frequent in Caucasians than African-American populations studied. WT: Patients with the wild-type genotype of the serotonin 2A receptor gene may have decreased response to certain antidepressants (i.e. citalopram) and increased risk of adverse drug reaction (i.e. anxiety, agitation, nausea/vomiting, drowsiness) when treated with certain SSRIs (i.e. citalopram , paroxetine). Other gene-drug variant associations include venlafaxine, fluvoxamine. (CPIC Level best drug: C/ PharmGKB Level Best drug: 3) Ref: 3, 7, 31 |
| HTR2A(rs6313) | HTR2A is a post-synaptic serotonin receptor that binds serotonin and is involved in amplification of excitatory signals to other neurons in the brain. Polymorphisms of this gene may affect antidepressant and antipsychotic response and risk of adverse effects. Mental Health: Patients with the mutant or heterozygous genotype of the serotonin 2A receptor gene (HTR2A-102) when treated for schizophrenia with olanzapine, may have an increased risk of weight gain compared to patients with the Wild Type genotype. Patients with the mutant or heterozygous genotype may also have a decreased risk of experiencing side effects to certain antidepressants (ex. paroxetine, citalopram) as compared to patients with the Wild Type genotype. (CPIC Level best drug: C/ PharmGKB Level Best drug:3)/ PharmGKB. Web site. Accessed November 1st, 2022. Ref: 3,12, 29, 30 |
| HTR2C(rs6318) | The HTR2C is a G-protein-coupled receptor, which responds to signaling through the neurotransmitter serotonin. Mutations of this gene may show association with mental illness and behavioral disorders and may be useful in predicting which patients are at risk for adverse events from certain psychiatric medications. Mental Health: HET/MUT: Patients who are heterozygous and mutant homozygous of the serotonin 2C receptor gene (HTR2C) may have increased neuropathic pain relief in men when treated with certain SSRIs (i.e. escitalopram {Lexapro}) and increased severity of weight gain when treated with antipsychotics (i.e. olanzapine {Zyprexa}) in people with schizophrenia. WT: Patients with the wild-type genotype of the serotonin 2C receptor is associated with decreased neuropathic pain relief when treated with certain SSRIs (i.e escitalopram) in men and not associated with increased weight gain when treated with antipsychotics (i.e. olanzapine ) in people with schizoaffective disorders. Other gene-drug variant associations inlcude Clozapine, risperidone.(CPIC Level best drug: C/ PharmGKB Level Best drug: 3) Ref: 3, 8, 13, 28. |
| IFNL3 | IFNL3, also called interferon, lambda 3, is the strongest baseline predictor of response to PEG-interferon-alpha-containing regimens in HCV genotype 1 patients. Patients with the favorable response genotype increased likelihood of response (higher SVR rate) to PEG-interferon-alpha-containing regimens as compared to patients with unfavorable response genotype. Consider implications before initiating PEG-IFN alpha and ribaviron (RBV) containing regimens. (www.pharmgkb.org/gene/PA166049147/clinicalAnnotation/ https://cpicpgx.org/guidelines/guideline-for-peg-interferon-alpha-based-regimens-and-ifnl3/ Accessed August 28th, 2022.) |
| ITGB3 | ITGB3 encodes the gene for beta 3 integrin, which is found on the surface of platelets. The ITGB3 gene is involved in several pathways and diseases related to platelet function and blood clotting. Mutations in this gene influence the efficacy of medications such as clopidogrel. Ref: 55, 56, 67 |
| MTHFR (both alleles) | The protein encoded by this gene catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a co-substrate for homocysteine remethylation to methionine. Mutations in this gene are associated with methylenetetrahydrofolate reductase deficiency. Genetic variation in this gene may influence susceptibility to occlusive vascular disease, neural tube defects, cancer. Mental Health: Patients who are homozygous mutant for MTHFR 677 (T/T) genotype may have an increased risk of early onset of schizophrenia, bipolar disorder, and increase in severity of depressive symptoms in depressive disorders. Ethnic populations studied include: African, Asian, Caucasian. Oncology/Rheumatology: Patients with AG or AA genotypes and treated for certain cancers (ex. lymphoma, osteocarcinoma, leukemia) and arthritis (ex. rheumatoid, psoriatic) may be at an increased risk of adverse effects if treated with methotrexate when compared to patients with GG genotype However, conflicting evidence has been reported. Other clinical and genetic factors may also influence risk of toxicity following methotrexate treatment. Cardiovascular: Individuals who are found to have two mutations of MTHFR may be at an increased risk for serious blood clot formation. Individuals who have only one or no copies of either genetic change in the MTHFR gene may still be at increased risk. Other changes in the MTHFR gene that were not tested for, changes in other genes, and non-genetic factors may still increase a patient’s risk for thrombosis. (CPIC Level best drug: C/ PharmGKB Level Best drug: 2A) (PharmGKB) Ref: 14, 15, 66, 68 |
| OPRM1 | Mu 1 opioid receptor (OPRM1) is a pharmacodynamic receptor that is partly responsible for opioid effectiveness and is associated with pain sensitivity, substance dependence and abuse. Pain: MUT: In several clinical studies, patients with the mu (μ) opioid receptor A118G mutant (GG) homozygous variant demonstrated increased pain responses and required higher doses (@90%) of oral morphine for cancer pain relief compared to the wild-type genotype and higher doses of other analgesics (i.e. fentanyl) for long-term treatment and in the acute postoperative setting. Effects were more pronounced in the Asian population versus Caucasians. In alcohol-dependent patients, carriers of the G allele have a lower relapse rate when treated with naltrexone. HET: In several clinical studies, patients with the mu (μ) opioid receptor A118G heterozygous (AG) variant may have a moderate increase in pain response and require slightly higher doses of oral morphine for cancer pain relief and other opioid analgesics (i.e. fentanyl) for long-term treatment and in the acute postoperative setting. In alcohol-dependent patients, carriers with the heterozygous variant may have a predicted lower relapse rate when treated with naltrexone. WT: Patients with the mu (μ) opioid receptor wild-type (AA) genotype should expect typical therapeutic response to opioid analgesics. Other genetic and clinical factors may also influence patient’s response to opioid medications. In alcohol-dependent patients with the wild-type genotype, these patients may not respond to naltrexone as expected. (CPIC Level best drug: C/ PharmGKB Level Best drug: 3) Ref: 16, 17, 18, 20 |
| OPRK1(rs1051660) | Kappa 1 opioid receptor (OPRK1) is a pharmacodynamic receptor that is partly responsible for opioid effectiveness and is associated with pain sensitivity, substance dependence and abuse. Ref: 3, 19 |
| SLC6A4 | This gene encodes an integral membrane protein that transports the neurotransmitter serotonin from synaptic spaces into presynaptic neurons. There are conflicting results in the literature about the possible effects that polymorphisms of this gene may have in behavior and depression. Mental Health: Low/Intermediate/High Activity: Polymorphisms of the S or short allele of serotonin transporter gene, SLC6A4, or, in combination with the LG long allele (Low activity), is associated with greater adverse drug reaction burden (i.e. anxiety, agitation, drowsiness) and/or decreased response to SSRI therapy (i.e. paroxetine (Paxil), citalopram (celexa), escitalopram, (lexapro) sertraline {Zoloft}). Polymorphisms with combinations of the S (short allele) and long alleles (LA, LG) {Intermediate activity}of the SLC6A4 gene may have greater adverse drug reaction burden (i.e. anxiety, agitation, drowsiness) and/or decreased response to SSRI therapy (i.e. paroxetine, citalopram, sertraline). Patients who are homozygous for the LA long allele of the SLC6A4 gene (High activity)should expect normal or typical response to SSRI antidepressants (i.e. paroxetine, citalopram, sertraline). (CPIC Level best drug: B-C/PharmGKB Level Best drug: 3). Ref: 3, 11 |
| SLCO1B1 | SLCO1B1 (also known as OAT1B1) encodes for the formation of influx transporter that moves medications into cells. Variations in SLCO1B1 may affect the blood levels of medications that are substrates for this transporter. Some examples of SLCO1B1 transported medications include: atorvastatin, bosentan, ezetimibe, fluvastatin, glyburide, SN-38 (active metabolite of irinotecan), rosuvastatin, simvastatin acid, pitavastatin, pravastatin, repaglinide, rifampin, valsartan, olmesartan. Ref: 3, 34, 65 |
| UGT1A1 | Uridine diphosphate (UDP)-glucuronosyl transferase 1A1 (UGT1A1) is an enzyme responsible for bilirubin conjugation with glucuronic acid that transforms small lipophilic molecules, such as steroids, bilirubin, hormones, and drugs, into water-soluble, excretable metabolites. Patients with reduced UGT1A1 enzyme activity are at risk for adverse outcomes with certain medications (ex. irinotecan, atazanavir). The FDA medication labels for nilotinib, pazopanib, and belinostat all contain warnings for an increased risk (incidence) of adverse outcomes in patients who have UGT1A1 alleles associated with reduced activity. Ref: 3, 57, 58, 59, 60, 61. |
| UGT2B15 | UDP-glucuronosyltransferase (UGT) 2B15 is a major drug glucuronidation enzyme expressed in human liver. The UGTs are of major importance in the conjugation and subsequent elimination of potentially toxic xenobiotics and endogenous compounds. Polymorphisms have been associated with variation in medication metabolism, including some medications used for mental health disorders, PPAR agonist (Thiazolidinediones), and clearance of oxazepam or lorazepam. Ref: 3, 62, 63. |
| VKORC1 | Vitamin K epoxide complex subunit 1 (VKORC1) is the enzyme that activates Vitamin K. Mutations in VKORC1 are associated with deficiencies in vitamin-K-dependent clotting factors. A particular VKORC1 variant (-1639G>A) leads to increased sensitivity to warfarin. VKORC1 mutation accounts for 25-44% of warfarin dose variability and is typically tested for at the same time as 2C9 when warfarin is being considered. Ref: 3, 39 |
References for individual gene-drug interactions are available at EffectiveRX Panel References.
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