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Pharmacogenetic tests, along with other information about patients and their disease or condition, can play an important role in drug therapy. When a health care provider is considering prescribing a drug, knowledge of a patient's genotype may be used to aid in determining a therapeutic strategy, determining an appropriate dosage, or assessing the likelihood of benefit or toxicity.

For the pharmacogenetic associations listed in this table, the FDA has evaluated and believes there is sufficient scientific evidence to suggest that subgroups of patients with certain genetic variants, or genetic variant-inferred phenotypes (such as affected subgroup in the table below), are likely to have altered drug metabolism, and in certain cases, differential therapeutic effects, including differences in risks of adverse events.

The fact that the FDA has included a particular gene-drug interaction in the table does not necessarily mean the FDA advocates using a pharmacogenetic test before prescribing the corresponding medication, unless the test is a companion diagnostic. Tests that are essential for the safe and effective use of a therapeutic product, including those that identify patients for which the drug is contraindicated, are companion diagnostics.

This table is not intended to affect current regulatory requirements or policies, including the FDA's policy regarding companion diagnostics: Guidance for Industry and FDA Staff: In Vitro Companion Diagnostic Devices. Nor is the table intended to make an assessment on the safe and effective use of, or regulatory requirements for, tests that detect variants in the referenced genes, or to provide comprehensive information on the described gene-drug interactions.

Specific information regarding therapeutic management is provided for some pharmacogenetic associations listed in the table, but most of the associations listed have not been evaluated in terms of the impact of genetic testing on clinical outcomes, such as improved therapeutic effectiveness or increased risk of specific adverse events. In addition, clinical studies, if available, may only have linked genetic variation to a drug's pharmacokinetics (such as the way in which the drug is metabolized), and differences in drug efficacy or safety across different genotype subgroups may not be known. If no statements related to efficacy or toxicity are provided, the scientific evidence the FDA reviewed was considered insufficient to support such associations.

The FDA recognizes that practitioners will take into account different sources and strengths of evidence and will make prescribing decisions based on their judgment about which treatments are appropriate for individual patients. In particular, each patient's genetic makeup is only one of many factors that may impact drug concentrations and response, highlighting the fact that information provided in this table is limited to certain pharmacogenetic associations only and does not provide comprehensive information needed for safe and effective use of a drug. Accordingly, health care providers should refer to FDA-approved labeling for prescribing information, including monitoring instructions and information on other factors that may affect drug concentrations, benefits, and risks. In this context, the information in this Table is intended primarily for prescribers, and patients should not adjust their medications without consulting their prescriber.

This version of the table is limited to pharmacogenetic associations that are related to drug metabolizing enzyme gene variants, drug transporter gene variants, and gene variants that have been related to a predisposition for certain adverse events. The FDA recognizes that various other pharmacogenetic associations exist that are not listed here, and this table will be updated periodically with additional pharmacogenetic associations supported by sufficient scientific evidence.

+ The table describes gene-drug interactions and indicates specific affected subgroup(s) to which the interaction applies. The affected subgroup(s) may be carriers of a specific genetic variant (for example, HLA-B*15:02), or a genotype-inferred phenotype, ultrarapid, normal, intermediate, or poor metabolizers/function transporters of a drug metabolizing enzyme/drug transporter. Normal metabolizers or normal transporters do not have genetic variants that are expected to impact metabolism or transport function. In general, ultrarapid metabolizers have two or more copies of a genetic variant that increases metabolic function; intermediate metabolizers or reduced function transporters are individuals who have one or two copies of a genetic variant that reduces the ability to metabolize or transport a drug; and poor metabolizers or poor function transporters are individuals who generally have two copies of a genetic variant that results in little to no ability to metabolize or transport a drug.

In some cases, a specific genetic variant may affect the metabolism of different drugs in different ways. In cases where the association is limited to specific genetic variants and does not apply to all individuals with the genotype-inferred phenotype, the specific variants are provided in the table. In cases where individual genetic variants are not listed in the table, the FDA believes there is sufficient scientific evidence to generally support the described association for the genotype-inferred phenotype subgroup, provided specific genetic variants are determined to confer the genotype-inferred phenotype based on sufficient scientific evidence.

For example, when considering, as described in the table, that poor and intermediate metabolizers of CYP2C19 have higher systemic active metabolite concentrations, higher adverse reaction risk, and dosage adjustments are recommended when taking clobazam, sufficient scientific evidence supports the following, with respect to the *2 allele:

The Punnett square is a square diagram that is used to predict the genotypes of a particular cross or breeding experiment. It is named after Reginald C. Punnett, who devised the approach in 1905.[3][4][5][6][7][8] The diagram is used by biologists to determine the probability of an offspring having a particular genotype. The Punnett square is a tabular summary of possible combinations of maternal alleles with paternal alleles.[9] These tables can be used to examine the genotypical outcome probabilities of the offspring of a single trait (allele), or when crossing multiple traits from the parents.

The Punnett square is a visual representation of Mendelian inheritance, a fundamental concept in genetics which is discovery of Gregor Mendel.[10] For multiple traits, using the "forked-line method" is typically much easier than the Punnett square. Phenotypes may be predicted with at least better-than-chance accuracy using a Punnett square, but the phenotype that may appear in the presence of a given genotype can in some instances be influenced by many other factors, as when polygenic inheritance and/or epigenetics are at work.

Zygosity refers to the grade of similarity between the alleles that determine one specific trait in an organism. In its simplest form, a pair of alleles can be either homozygous or heterozygous. Homozygosity, with homo relating to same while zygous pertains to a zygote, is seen when a combination of either two dominant or two recessive alleles code for the same trait. Recessive are always lowercase letters. For example, using 'A' as the representative character for each allele, a homozygous dominant pair's genotype would be depicted as 'AA', while homozygous recessive is shown as 'aa'. Heterozygosity, with hetero associated with different, can only be 'Aa' (the capital letter is always presented first by convention). The phenotype of a homozygous dominant pair is 'A', or dominant, while the opposite is true for homozygous recessive. Heterozygous pairs always have a dominant phenotype.[11] To a lesser degree, hemizygosity[12] and nullizygosity[13] can also be seen in gene pairs.

"Mono-" means "one"; this cross indicates that the examination of a single trait. This could mean (for example) eye color. Each genetic locus is always represented by two letters. So in the case of eye color, say "B = Brown eyes" and "b = green eyes". In this example, both parents have the genotype Bb. For the example of eye color, this would mean they both have brown eyes. They can produce gametes that contain either the B or the b allele. (It is conventional in genetics to use capital letters to indicate dominant alleles and lower-case letters to indicate recessive alleles.) The probability of an individual offspring's having the genotype BB is 25%, Bb is 50%, and bb is 25%. The ratio of the phenotypes is 3:1, typical for a monohybrid cross. When assessing phenotype from this, "3" of the offspring have "Brown" eyes and only one offspring has "green" eyes. (3 are "B?" and 1 is "bb")

The way in which the B and b alleles interact with each other to affect the appearance of the offspring depends on how the gene products (proteins) interact (see Mendelian inheritance). This can include lethal effects and epistasis (where one allele masks another, regardless of dominant or recessive status).

More complicated crosses can be made by looking at two or more genes. The Punnett square works, however, only if the genes are independent of each other, which means that having a particular allele of gene "A" does not alter the probability of possessing an allele of gene "B". This is equivalent to stating that the genes are not linked, so that the two genes do not tend to sort together during meiosis.

Since dominant traits mask recessive traits (assuming no epistasis), there are nine combinations that have the phenotype round yellow, three that are round green, three that are wrinkled yellow, and one that is wrinkled green. The ratio 9:3:3:1 is the expected outcome when crossing two double-heterozygous parents with unlinked genes. Any other ratio indicates that something else has occurred (such as lethal alleles, epistasis, linked genes, etc.).

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