PharmGKB contains no dosing guidelines for this drug/small molecule. To report known genotype-based dosing guidelines, or if you are interested in developing guidelines, click here.
PharmGKB annotates drug labels containing pharmacogenetic information approved by the US Food and Drug Administration (FDA), European Medicines Agency (EMA) and the Pharmaceuticals and Medical Devices Agency, Japan (PMDA). PharmGKB annotations provide a brief summary of the PGx in the label, an excerpt from the label and a downloadable highlighted label PDF file. A list of genes and phenotypes found within the label is mapped to label section headers and listed at the end of each annotation. PharmGKB also attempts to interpret the level of action implied in each label with the "PGx Level" tag.
- FDA Information is gathered from the FDA's "Table of Pharmacogenomic Biomarkers in Drug Labels" and from FDA-approved labels brought to our attention. Please note that drugs may be removed from or added to the FDA's Table without our knowledge. We periodically check the Table for changes and update PharmGKB accordingly. Drugs listed on the Table to our knowledge are tagged with the Biomarker icon. A drug label that has been removed from the Table will not have the Biomarker icon but will continue to have an annotation on PharmGKB stating the label has been removed from the FDA's Table. We acquire label PDF files from DailyMed.
- EMA European Public Assessment Reports (EPARs) that contain PGx information were identified from [Article:24433361] and also by searching for drugs for which we have PGx-containing FDA drug labels.
- PMDA Japanese drug label annotation information is sourced from Shimazawa and Ikeda (2013), whose paper provided translations of the pharmacogenetic information contained in PMDA package inserts. The authors selected which PMDA package inserts to examine for PGx information based the FDA's "Table of Pharmacogenomic Biomarkers in Drug Labels".
We welcome any information regarding drug labels containing PGx information approved by the FDA, EMA, PMDA or other Medicine Agencies around the world - please contact feedback.
Tretinoin is a derivative of vitamin A (retinol) used for the treatment of skin conditions and acute promyelocytic leukemia (APL). APL is characterized by the translocation t(15;17) and PML/RAR alpha (RARA) fusion protein.
Excerpt from the tretinoin (Vesanoid) label:
Confirmation of the diagnosis of APL should be sought by detection of the t(15;17) genetic marker by cytogenetic studies. If these are negative, PML/RAR alpha fusion should be sought using molecular diagnostic techniques. The response rate of other AML subtypes to VESANOID has not been demonstrated; therefore, patients who lack the genetic marker should be considered for alternative treatment.
For the complete drug label text with sections containing pharmacogenetic information highlighted, see the tretinoin (Vesanoid) drug label.
*Disclaimer: The contents of this page have not been endorsed by the FDA and are the sole responsibility of PharmGKB.
Genes and/or phenotypes found in this label
Tretinoin is indicated for the treatment of acute promyelocytic leukemia (APL). The PMDA package insert for tretinoin notes that it acts on the PML-RARa fusion gene, allowing immature promyelocytes to differentiate into normal mature blood cells.
Please note that the information contained within this drug label annotation is sourced from Shimazawa and Ikeda (2013), whose paper provided an unofficial translation of the pharmacogenetic information contained in the PMDA package insert for research purposes.
Excerpt from the package insert for tretinoin:
Mechanism of action: PML-RAR-a fusion gene is presumed responsible for preventing APL chimeric cells from differentiating into more mature cells. Tretinoin acts on PML-RAR to lift this block, causing the immature promyelocytes to differentiate to normal mature blood cells.
For the complete drug label text with sections containing pharmacogenetic information highlighted, see the tretinoin package insert (in Japanese).
*Disclaimer: The contents of this page have not been endorsed by the PMDA and are the sole responsibility of PharmGKB.
Genes and/or phenotypes found in this label
PharmGKB contains no Clinical Variants that meet the highest level of criteria.
Disclaimer: The PharmGKB's clinical annotations reflect expert consensus based on clinical evidence and peer-reviewed literature available at the time they are written and are intended only to assist clinicians in decision-making and to identify questions for further research. New evidence may have emerged since the time an annotation was submitted to the PharmGKB. The annotations are limited in scope and are not applicable to interventions or diseases that are not specifically identified.
The annotations do not account for individual variations among patients, and cannot be considered inclusive of all proper methods of care or exclusive of other treatments. It remains the responsibility of the health-care provider to determine the best course of treatment for a patient. Adherence to any guideline is voluntary, with the ultimate determination regarding its application to be made solely by the clinician and the patient. PharmGKB assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the PharmGKB clinical annotations, or for any errors or omissions.
- All Trans Retinoic Acid
- All Trans-Retinoic Acid
- Retionic Acid
- beta-Retinoic Acid
- Stieva-a Forte
Tretinoin, also known as all-trans-retinoic acid (ATRA), is a naturally occurring derivative of vitamin A (retinol). Retinoids such as tretinoin are important regulators of cell reproduction, proliferation, and differentiation and are used to treat acne and photodamaged skin and to manage keratinization disorders such as ichthyosis and keratosis follicularis. Tretinoin also represents the class of anticancer drugs called differentiating agents and is used in the treatment of acute promyelocytic leukemia (APL).
Source: Drug Bank
For the the induction of remission in patients with acute promyelocytic leukemia (APL), French-American-British (FAB) classification M3 (including the M3 variant); For the topical treatment of acne vulgaris, flat warts and other skin conditions (psoriasis, ichthyosis congenita, icthyosis vulgaris, lamellar icthyosis, keratosis palmaris et plantaris, epidermolytic hyperkeratosis, senile comedones, senile keratosis, keratosis follicularis (Darier's disease), and basal cell carcinomas.); For palliative therapy to improve fine wrinkling, mottled hyperpigmentation, roughness associated with photodamage.
Source: Drug Bank
Information pulled from DrugBank has not been reviewed by PharmGKB.
Pharmacology, Interactions, and Contraindications
Mechanism of Action
Tretinoin binds to alpha, beta, and gamma retinoic acid receptors (RARs). RAR-alpha and RAR-beta have been associated with the development of acute promyelocytic leukemia and squamous cell cancers, respectively. RAR-gamma is associated with retinoid effects on mucocutaneous tissues and bone. Although the exact mechanism of action of tretinoin is unknown, current evidence suggests that the effectiveness of tretinoin in acne is due primarily to its ability to modify abnormal follicular keratinization. Comedones form in follicles with an excess of keratinized epithelial cells. Tretinoin promotes detachment of cornified cells and the enhanced shedding of corneocytes from the follicle. By increasing the mitotic activity of follicular epithelia, tretinoin also increases the turnover rate of thin, loosely-adherent corneocytes. Through these actions, the comedo contents are extruded and the formation of the microcomedo, the precursor lesion of acne vulgaris, is reduced. Tretinoin is not a cytolytic agent but instead induces cytodifferentiation and decreased proliferation of APL cells in culture and in vivo. When Tretinoin is given systemically to APL patients, tretinoin treatment produces an initial maturation of the primitive promyelocytes derived from the leukemic clone, followed by a repopulation of the bone marrow and peripheral blood by normal, polyclonal hematopoietic cells in patients achieving complete remission (CR). The exact mechanism of action of tretinoin in APL is unknown.
Source: Drug Bank
Tretinoin, also known as all-_trans_-retinoic acid (ATRA), is a naturally occurring derivative of vitamin A (retinol). Retinoids such as tretinoin are important regulators of cell reproduction, proliferation, and differentiation and are used to treat acne and photodamaged skin and to manage keratinization disorders such as ichthyosis and keratosis follicularis. Tretinoin also represents the class of anticancer drugs called differentiating agents and is used in the treatment of acute promyelocytic leukemia (APL).
Source: Drug Bank
Absorption, Distribution, Metabolism, Elimination & Toxicity
PharmGKB Curated Pathways
Pathways created internally by PharmGKB based primarily on literature evidence.
PharmGKB contains no curated pathways for this drug. If you would like to volunteer to work on a pathway, please let us know.
Links to non-PharmGKB pathways.
Publications related to tretinoin: 8
The following icons indicate that data of a certain type is available:
- DG Dosing Guideline information is available
- DL Drug Label information is available
- CA High-level Clinical Annotation is available
- VA Variant Annotation is available
- VIP VIP information is available
- PW Pathway is available
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These are trials that mention tretinoin and are related to either pharmacogenetics or pharmacogenomics.