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Identification
NameTretinoin
Accession NumberDB00755  (APRD00362, NUTR00051)
Typesmall molecule
Groupsapproved, investigational, nutraceutical
Description

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).

Structure
Thumb
Synonyms
SynonymLanguageCode
All Trans Retinoic AcidNot AvailableNot Available
All Trans-Retinoic AcidNot AvailableNot Available
ATRANot AvailableNot Available
Retionic AcidNot AvailableIS
TretinoinGermanINN
TretinoinaSpanishINN
TrétinoïneFrenchINN
TretinoinumLatinINN
Vitamin A acidNot AvailableIS
SaltsNot Available
Brand names
NameCompany
AberelJanssen
AberelaJanssen
AirolPierre Fabre Dermo
AmnesteemMylan Pharmaceuticals
ClaravisBarr Laboratories Inc.
DermairolRoche
EudynaZydus
KétrelBailleul
Retisol-AStiefel
SotretRanbaxy Laboratories Inc.
Stieva-AStiefel
VesanoidRoche
VitinoinNot Available
Brand mixtures
Brand NameIngredients
SolageMequinol and Tretinoin
Categories
CAS number302-79-4
WeightAverage: 300.4351
Monoisotopic: 300.20893014
Chemical FormulaC20H28O2
InChI KeyInChIKey=SHGAZHPCJJPHSC-YCNIQYBTSA-N
InChI
InChI=1S/C20H28O2/c1-15(8-6-9-16(2)14-19(21)22)11-12-18-17(3)10-7-13-20(18,4)5/h6,8-9,11-12,14H,7,10,13H2,1-5H3,(H,21,22)/b9-6+,12-11+,15-8+,16-14+
IUPAC Name
3,7-dimethyl-9-(2,6,6-trimethylcyclohex-1-en-1-yl)nona-2,4,6,8-tetraenoic acid
SMILES
CC(C=CC1=C(C)CCCC1(C)C)=CC=CC(C)=CC(O)=O
Mass SpecNot Available
Taxonomy
KingdomOrganic Compounds
SuperclassLipids
ClassPrenol Lipids
SubclassRetinoids
Direct parentRetinoids
Alternative parentsDiterpenes; Carbocyclic Fatty Acids; Branched Fatty Acids; Unsaturated Fatty Acids; Enones; Carboxylic Acids; Polyamines; Enolates
Substituentsenone; enolate; polyamine; carboxylic acid; carboxylic acid derivative
Classification descriptionThis compound belongs to the retinoids. These are compounds that are related to vitamin A, especially retinol.
Pharmacology
IndicationFor 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.
PharmacodynamicsTretinoin, 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).
Mechanism of actionTretinoin 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.
Absorption1-31% (topical)
Volume of distributionNot Available
Protein binding> 95%
Metabolism

Hepatic

SubstrateEnzymesProduct
Tretinoin
4-Hydroxyretinoic acidDetails
Tretinoin
18-Hydroxyretinoic acidDetails
Tretinoin
5,6-Epoxyretinoic acidDetails
Tretinoin
4-Oxoretinoic acidDetails
Tretinoin
    Retinoyl b-glucuronideDetails
    Tretinoin
      Retinyl beta-glucuronideDetails
      Route of eliminationNot Available
      Half life0.5-2 hours
      ClearanceNot Available
      ToxicityNot Available
      Affected organisms
      • Humans and other mammals
      PathwaysNot Available
      SNP Mediated EffectsNot Available
      SNP Mediated Adverse Drug ReactionsNot Available
      ADMET
      Predicted ADMET features
      Property Value Probability
      Human Intestinal Absorption + 0.9925
      Blood Brain Barrier + 0.9311
      Caco-2 permeable + 0.7603
      P-glycoprotein substrate Non-substrate 0.6144
      P-glycoprotein inhibitor I Non-inhibitor 0.8912
      P-glycoprotein inhibitor II Non-inhibitor 0.8088
      Renal organic cation transporter Non-inhibitor 0.8639
      CYP450 2C9 substrate Non-substrate 0.8221
      CYP450 2D6 substrate Non-substrate 0.9115
      CYP450 3A4 substrate Substrate 0.6025
      CYP450 1A2 substrate Non-inhibitor 0.9046
      CYP450 2C9 substrate Non-inhibitor 0.8831
      CYP450 2D6 substrate Non-inhibitor 0.9231
      CYP450 2C19 substrate Non-inhibitor 0.9025
      CYP450 3A4 substrate Non-inhibitor 0.9301
      CYP450 inhibitory promiscuity Low CYP Inhibitory Promiscuity 0.9252
      Ames test Non AMES toxic 0.8944
      Carcinogenicity Non-carcinogens 0.7081
      Biodegradation Ready biodegradable 0.5554
      Rat acute toxicity 2.1455 LD50, mol/kg Not applicable
      hERG inhibition (predictor I) Weak inhibitor 0.9562
      hERG inhibition (predictor II) Non-inhibitor 0.9538
      Pharmacoeconomics
      Manufacturers
      • Hoffmann la roche inc
      • Genpharm inc
      • Barr laboratories inc
      • Ranbaxy pharmaceuticals inc
      • Ranbaxy laboratories ltd
      • Mylan bertek pharmaceuticals inc
      • Ortho dermatologics
      • Johnson and johnson consumer companies inc
      • Spear pharmaceuticals inc
      • Triax pharmaceuticals llc
      • Dow pharmaceutical sciences inc
      • Mylan pharmaceuticals inc
      • Teva pharmaceuticals usa
      • Wockhardt eu operations (swiss) ag
      • Ranbaxy Pharmaceuticals Inc.
      Packagers
      Dosage forms
      FormRouteStrength
      CapsuleOral
      CreamTopical
      GelTopical
      LiquidTopical
      Prices
      Unit descriptionCostUnit
      Tretinoin (Emollient) 0.05% Cream 60 gm Tube200.07USDtube
      Tri-Luma 0.01-4-0.05% Cream 30 gm Tube199.99USDtube
      Solage 2-0.01% Solution 30ml Bottle168.67USDbottle
      Tretinoin (Emollient) 0.05% Cream 40 gm Tube135.99USDtube
      Tretinoin 0.1% Cream 45 gm Tube114.16USDtube
      Tretinoin 0.025% Gel 45 gm Tube99.64USDtube
      Tretinoin 0.01% Gel 45 gm Tube98.85USDtube
      Tretinoin 0.05% Cream 45 gm Tube97.94USDtube
      Tretinoin 0.025% Cream 45 gm Tube83.97USDtube
      Tretinoin acid powder74.21USDg
      Tretinoin 0.1% Cream 20 gm Tube60.96USDtube
      Tretinoin 0.05% Cream 20 gm Tube52.23USDtube
      Tretinoin 0.025% Cream 20 gm Tube44.36USDtube
      Tretinoin 0.025% Gel 15 gm Tube42.26USDtube
      Tretinoin 0.01% Gel 15 gm Tube35.99USDtube
      Vesanoid 10 mg capsule30.32USDcapsule
      Accutane 40 mg capsule27.62USDcapsule
      Tretinoin 10 mg capsule27.29USDcapsule
      Accutane 20 mg capsule23.77USDcapsule
      Amnesteem 40 mg capsule22.6USDcapsule
      Claravis 40 mg capsule21.73USDcapsule
      Accutane 10 mg capsule20.05USDcapsule
      Amnesteem 20 mg capsule19.45USDcapsule
      Claravis 20 mg capsule18.7USDcapsule
      Claravis 30 mg capsule16.78USDcapsule
      Amnesteem 10 mg capsule16.4USDcapsule
      Claravis 10 mg capsule15.77USDcapsule
      Sotret 40 mg capsule10.08USDcapsule
      Sotret 20 mg capsule8.67USDcapsule
      Sotret 30 mg capsule8.44USDcapsule
      Sotret 10 mg capsule7.31USDcapsule
      Tri-luma cream6.4USDg
      Retin-a micro 0.04% gel5.65USDg
      Retin-a micro 0.1% gel5.65USDg
      Solage topical solution5.59USDml
      Retin-a micro pump 0.04% gel4.74USDg
      Retin-a micro pump 0.1% gel4.74USDg
      Retin-a 0.05% cream4.64USDg
      Retin-a 0.1% cream4.51USDg
      Renova 0.02% cream4.46USDg
      Renova pump 0.02% cream4.28USDg
      Retin-a 0.025% cream4.14USDg
      Refissa 0.05% cream3.6USDg
      Tretinoin 0.05% emollient crm3.38USDg
      Avita 0.025% cream3.19USDg
      Tretinoin 0.1% cream2.36USDg
      Tretinoin 0.025% cream2.17USDg
      Tretinoin 0.05% cream2.02USDg
      DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
      Patents
      CountryPatent NumberApprovedExpires (estimated)
      United States63530292000-08-242020-08-24
      United States54705671993-03-192010-03-19
      Properties
      Statesolid
      Experimental Properties
      PropertyValueSource
      melting point181 °CPhysProp
      water solubility<0.1 g/100 mLNot Available
      logP6.30HANSCH,C ET AL. (1995)
      Predicted Properties
      PropertyValueSource
      water solubility4.77e-03 g/lALOGPS
      logP5.66ALOGPS
      logP5.01ChemAxon
      logS-4.8ALOGPS
      pKa (strongest acidic)5ChemAxon
      physiological charge-1ChemAxon
      hydrogen acceptor count2ChemAxon
      hydrogen donor count1ChemAxon
      polar surface area37.3ChemAxon
      rotatable bond count5ChemAxon
      refractivity97.79ChemAxon
      polarizability36.62ChemAxon
      number of rings1ChemAxon
      bioavailability1ChemAxon
      rule of fiveNoChemAxon
      Ghose filterYesChemAxon
      Veber's ruleYesChemAxon
      MDDR-like ruleNoChemAxon
      Spectra
      Spectra
      References
      Synthesis ReferenceNot Available
      General Reference
      1. Huang ME, Ye YC, Chen SR, Chai JR, Lu JX, Zhoa L, Gu LJ, Wang ZY: Use of all-trans retinoic acid in the treatment of acute promyelocytic leukemia. Blood. 1988 Aug;72(2):567-72. Pubmed
      2. Castaigne S, Chomienne C, Daniel MT, Ballerini P, Berger R, Fenaux P, Degos L: All-trans retinoic acid as a differentiation therapy for acute promyelocytic leukemia. I. Clinical results. Blood. 1990 Nov 1;76(9):1704-9. Pubmed
      3. Sanz MA: Treatment of acute promyelocytic leukemia. Hematology Am Soc Hematol Educ Program. 2006;:147-55. Pubmed
      4. Mao JT, Goldin JG, Dermand J, Ibrahim G, Brown MS, Emerick A, McNitt-Gray MF, Gjertson DW, Estrada F, Tashkin DP, Roth MD: A pilot study of all-trans-retinoic acid for the treatment of human emphysema. Am J Respir Crit Care Med. 2002 Mar 1;165(5):718-23. Pubmed
      5. Roth MD, Connett JE, D’Armiento JM, Foronjy RF, Friedman PJ, Goldin JG, Louis TA, Mao JT, Muindi JR, O’Connor GT, Ramsdell JW, Ries AL, Scharf SM, Schluger NW, Sciurba FC, Skeans MA, Walter RE, Wendt CH, Wise RA: Feasibility of retinoids for the treatment of emphysema study. Chest. 2006 Nov;130(5):1334-45. Pubmed
      External Links
      ResourceLink
      KEGG DrugD00094
      KEGG CompoundC00777
      PubChem Compound444795
      PubChem Substance46504843
      ChemSpider5337
      ChEBI15367
      ChEMBLCHEMBL38
      Therapeutic Targets DatabaseDNC000117
      PharmGKBPA451746
      Drug Product Database2243914
      RxListhttp://www.rxlist.com/cgi/generic/tretinoin.htm
      Drugs.comhttp://www.drugs.com/cdi/tretinoin.html
      WikipediaTretinoin
      ATC CodesD10AD01D10AD51L01XX14D10BA01D10AD04
      AHFS Codes
      • 92:00.00
      • 84:16.00
      PDB Entries
      FDA labelshow(42.8 KB)
      MSDSshow(29.1 KB)
      Interactions
      Drug Interactions
      Drug
      AtazanavirThe strong CYP2C8 inhibitor, Atazanavir, may decrease the metabolism and clearance of oral Tretinoin. Consider alternate therapy or monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Atazanavir is initiated, discontinued to dose changed.
      CarbamazepineThe strong CYP2C8 inducer, Carbamazepine, may increase the metabolism and clearance of oral Tretinoin. Consider alternate therapy to avoid failure of Tretinoin therapy or monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Carbamazepine is initiated, discontinued or dose changed.
      CelecoxibThe moderate CYP2C8 inhibitor, Celecoxib, may decrease the metabolism and clearance of oral Tretinoin. Monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Celecoxib is initiated, discontinued to dose changed.
      DemeclocyclineDemeclocycline may increase the adverse effects of oral Tretinoin. Increased risk of pseudotumour cerebri. Concurrent therapy should be avoided.
      DesogestrelOral Tretinoin may decrease the effect of oral contraceptive, Desogestrel. An alternate form of contraception should be used during concomitant therapy.
      DoxycyclineDoxycycline may increase the adverse effects of oral Tretinoin. Increase risk of pseudotumour cerebri. Concurrent therapy should be avoided.
      DrospirenoneOral Tretinoin may decrease the effect of oral contraceptive, Drospirenone. An alternate form of contraception should be used during concomitant therapy.
      EltrombopagThe moderate CYP2C8 inhibitor, Eltrombopag, may decrease the metabolism and clearance of oral Tretinoin. Monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Eltrombopag is initiated, discontinued or dose changed.
      Ethinyl EstradiolOral Tretinoin may decrease the effect of the oral contraceptive, Ethinyl Estradiol. An alternate form of contraception should be used during concomitant therapy.
      EthynodiolOral Tretinoin may decrease the effect of oral contraceptive, Ethynodiol Diacetate. An alternate form of contraception should be used during concomitant therapy.
      EtonogestrelOral Tretinoin may decrease the effect of oral contraceptive, Etonogestrel. An alternate form of contraception should be used during concomitant therapy.
      FelodipineThe moderate CYP2C8 inhibitor, Felopidine, may decrease the metabolism and clearance of oral Tretinoin. Monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Felopidine is initiated, discontinued to dose changed.
      FosphenytoinThe strong CYP2C8 inducer, Fosphenytoin, may increase the metabolism and clearance of oral Tretinoin. Consider alternate therapy to avoid failure of Tretinoin therapy or monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Fosphenytoin is initiated, discontinued or dose changed.
      GemfibrozilThe strong CYP2C8 inhibitor, Gemfibrozil, may decrease the metabolism and clearance of oral Tretinoin. Consider alternate therapy or monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Gemfibrozil is initiated, discontinued to dose changed.
      IrbesartanThe moderate CYP2C8 inhibitor, Irbesartan, may decrease the metabolism and clearance of oral Tretinoin. Monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Irbesartan is initiated, discontinued to dose changed.
      LapatinibThe moderate CYP2C8 inhibitor, Lapatinib, may decrease the metabolism and clearance of oral Tretinoin. Monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Lapatinib is initiated, discontinued to dose changed.
      LevonorgestrelOral Tretinoin may decrease the effect of oral contraceptive, Levonorgestrel. An alternate form of contraception should be used during concomitant therapy.
      LosartanThe moderate CYP2C8 inhibitor, Losartan, may decrease the metabolism and clearance of oral Tretinoin. Monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Losartan is initiated, discontinued to dose changed.
      MestranolOral Tretinoin may decrease the effect of oral contraceptive, Mestranol. An alternate form of contraception should be used during concomitant therapy.
      MinocyclineMinocycline may increase the adverse effects of oral Tretinoin. Increase risk of pseudotumour cerebri. Concurrent therapy should be avoided.
      NatalizumabOral tretinoin may increase the adverse/toxic effects of Natalizumab. Concurrent therapy should be avoided.
      NilotinibThe moderate CYP2C8 inhibitor, Nilotinib, may decrease the metabolism and clearance of oral Tretinoin. Monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Nilotinib is initiated, discontinued to dose changed.
      NorethindroneOral Tretinoin may decrease the effect of oral contraceptive, Norethindrone. An alternate form of contraception should be used during concomitant therapy.
      NorgestimateOral Tretinoin may decrease the effect of oral contraceptive, Norgestimate. An alternate form of contraception should be used during concomitant therapy.
      OxytetracyclineOxytetracycline may increase the adverse effects of oral Tretinoin. Increase risk of pseudotumour cerebri. Concurrent therapy should be avoided.
      PhenobarbitalThe strong CYP2C8 inducer, Phenobarbital, may increase the metabolism and clearance of oral Tretinoin. Consider alternate therapy to avoid failure of Tretinoin therapy or monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Phenobarbital is initiated, discontinued or dose changed.
      PhenytoinThe strong CYP2C8 inducer, Phenytoin, may increase the metabolism and clearance of oral Tretinoin. Consider alternate therapy to avoid failure of Tretinoin therapy or monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Phenytoin is initiated, discontinued or dose changed.
      PioglitazoneThe moderate CYP2C8 inhibitor, Pioglitazone, may decrease the metabolism and clearance of oral Tretinoin. Monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Pioglitazone is initiated, discontinued to dose changed.
      PrimidoneThe strong CYP2C8 inducer, Primidone, may increase the metabolism and clearance of oral Tretinoin. Consider alternate therapy to avoid failure of Tretinoin therapy or monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Primidone is initiated, discontinued or dose changed.
      QuinineThe moderate CYP2C8 inhibitor, Quinine, may decrease the metabolism and clearance of oral Tretinoin. Monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Quinine is initiated, discontinued to dose changed.
      RabeprazoleThe moderate CYP2C8 inhibitor, Rabaprazole, may decrease the metabolism and clearance of oral Tretinoin. Monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Rabaprazole is initiated, discontinued to dose changed.
      RifampicinThe strong CYP2C8 inducer, Rifampin, may increase the metabolism and clearance of oral Tretinoin. Consider alternate therapy to avoid failure of Tretinoin therapy or monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Rifampin is initiated, discontinued or dose changed.
      RifapentineThe strong CYP2C8 inducer, Rifapentine, may increase the metabolism and clearance of oral Tretinoin. Consider alternate therapy to avoid failure of Tretinoin therapy or monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Rifapentine is initiated, discontinued or dose changed.
      RitonavirThe strong CYP2C8 inhibitor, Ritonavir, may decrease the metabolism and clearance of oral Tretinoin. Consider alternate therapy or monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Ritonavir is initiated, discontinued to dose changed.
      RosiglitazoneThe moderate CYP2C8 inhibitor, Rosiglitazone, may decrease the metabolism and clearance of oral Tretinoin. Monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Rosiglitazone is initiated, discontinued to dose changed.
      SecobarbitalThe strong CYP2C8 inducer, Secobarbital, may increase the metabolism and clearance of oral Tretinoin. Consider alternate therapy to avoid failure of Tretinoin therapy or monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Secobarbital is initiated, discontinued or dose changed.
      SorafenibThe strong CYP2C8 inhibitor, Sorafenib, may decrease the metabolism and clearance of oral Tretinoin. Consider alternate therapy or monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Sorafenib is initiated, discontinued to dose changed.
      TamoxifenThe moderate CYP2C8 inhibitor, Tamoxifen, may decrease the metabolism and clearance of oral Tretinoin. Monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Tamoxifen is initiated, discontinued to dose changed.
      TetracyclineDemeclocycline may increase the adverse effects of oral Tretinoin. Increase risk of pseudotumour cerebri. Concurrent therapy should be avoided.
      TigecyclineDemeclocycline may increase the adverse effects of oral Tretinoin. Increase risk of pseudotumour cerebri. Concurrent therapy should be avoided.
      TrastuzumabIncreased risk of leukopenia and anemia due to synergistic effects. Monitor for signs and symptoms of adverse events during concomitant therapy.
      TrimethoprimThe moderate CYP2C8 inhibitor, Trimethoprim, may decrease the metabolism and clearance of oral Tretinoin. Monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Trimethoprim is initiated, discontinued to dose changed.
      Vitamin ATretinoin increases the risk of vitamin A toxicity. Avoid vitamin A supplementation while taking systemic tretinoin.
      Food InteractionsNot Available

      1. Retinoic acid receptor RXR-beta

      Kind: protein

      Organism: Human

      Pharmacological action: yes

      Actions: agonist

      Components

      Name UniProt ID Details
      Retinoic acid receptor RXR-beta P28702 Details

      References:

      1. Stafslien DK, Vedvik KL, De Rosier T, Ozers MS: Analysis of ligand-dependent recruitment of coactivator peptides to RXRbeta in a time-resolved fluorescence resonance energy transfer assay. Mol Cell Endocrinol. 2007 Jan 29;264(1-2):82-9. Epub 2006 Dec 20. Pubmed
      2. Redfern CP: Enhancing enhancers: new complexities in the retinoid regulation of gene expression. Biochem J. 2004 Oct 1;383(Pt 1):e1-2. Pubmed
      3. Nagasawa H, Takahashi S, Kobayashi A, Tazawa H, Tashima Y, Sato K: Effect of retinoic acid on murine preosteoblastic MC3T3-E1 cells. J Nutr Sci Vitaminol (Tokyo). 2005 Oct;51(5):311-8. Pubmed
      4. Schrage K, Koopmans G, Joosten EA, Mey J: Macrophages and neurons are targets of retinoic acid signaling after spinal cord contusion injury. Eur J Neurosci. 2006 Jan;23(2):285-95. Pubmed
      5. Hoegberg P, Schmidt CK, Fletcher N, Nilsson CB, Trossvik C, Gerlienke Schuur A, Brouwer A, Nau H, Ghyselinck NB, Chambon P, Hakansson H: Retinoid status and responsiveness to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in mice lacking retinoid binding protein or retinoid receptor forms. Chem Biol Interact. 2005 Sep 10;156(1):25-39. Pubmed

      2. Retinoic acid receptor RXR-gamma

      Kind: protein

      Organism: Human

      Pharmacological action: yes

      Actions: agonist

      Components

      Name UniProt ID Details
      Retinoic acid receptor RXR-gamma P48443 Details

      References:

      1. Koda T, Imai H, Morita M: Antiestrogenic activity of vitamin A in in vivo uterotrophic assay. Life Sci. 2007 Feb 13;80(10):945-9. Epub 2006 Nov 22. Pubmed
      2. He JC, Lu TC, Fleet M, Sunamoto M, Husain M, Fang W, Neves S, Chen Y, Shankland S, Iyengar R, Klotman PE: Retinoic acid inhibits HIV-1-induced podocyte proliferation through the cAMP pathway. J Am Soc Nephrol. 2007 Jan;18(1):93-102. Epub 2006 Dec 20. Pubmed
      3. Day RM, Lee YH, Park AM, Suzuki YJ: Retinoic acid inhibits airway smooth muscle cell migration. Am J Respir Cell Mol Biol. 2006 Jun;34(6):695-703. Epub 2006 Feb 2. Pubmed
      4. Schrage K, Koopmans G, Joosten EA, Mey J: Macrophages and neurons are targets of retinoic acid signaling after spinal cord contusion injury. Eur J Neurosci. 2006 Jan;23(2):285-95. Pubmed
      5. Wang J, Yen A: A novel retinoic acid-responsive element regulates retinoic acid-induced BLR1 expression. Mol Cell Biol. 2004 Mar;24(6):2423-43. Pubmed

      3. Retinoic acid receptor gamma

      Kind: protein

      Organism: Human

      Pharmacological action: yes

      Actions: agonist

      Components

      Name UniProt ID Details
      Retinoic acid receptor gamma P13631 Details

      References:

      1. Overington JP, Al-Lazikani B, Hopkins AL: How many drug targets are there? Nat Rev Drug Discov. 2006 Dec;5(12):993-6. Pubmed
      2. Imming P, Sinning C, Meyer A: Drugs, their targets and the nature and number of drug targets. Nat Rev Drug Discov. 2006 Oct;5(10):821-34. Pubmed
      3. Reddy AP, Chen JY, Zacharewski T, Gronemeyer H, Voorhees JJ, Fisher GJ: Characterization and purification of human retinoic acid receptor-gamma 1 overexpressed in the baculovirus-insect cell system. Biochem J. 1992 Nov 1;287 ( Pt 3):833-40. Pubmed
      4. Kamei Y, Kawada T, Kazuki R, Sugimoto E: Retinoic acid receptor gamma 2 gene expression is up-regulated by retinoic acid in 3T3-L1 preadipocytes. Biochem J. 1993 Aug 1;293 ( Pt 3):807-12. Pubmed
      5. Borger DR, Mi Y, Geslani G, Zyzak LL, Batova A, Engin TS, Pirisi L, Creek KE: Retinoic acid resistance at late stages of human papillomavirus type 16-mediated transformation of human keratinocytes arises despite intact retinoid signaling and is due to a loss of sensitivity to transforming growth factor-beta. Virology. 2000 May 10;270(2):397-407. Pubmed
      6. Berman HM, Westbrook J, Feng Z, Gilliland G, Bhat TN, Weissig H, Shindyalov IN, Bourne PE: The Protein Data Bank. Nucleic Acids Res. 2000 Jan 1;28(1):235-42. Pubmed
      7. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. Pubmed

      4. Retinal dehydrogenase 1

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Components

      Name UniProt ID Details
      Retinal dehydrogenase 1 P00352 Details

      References:

      1. Mic FA, Molotkov A, Molotkova N, Duester G: Raldh2 expression in optic vesicle generates a retinoic acid signal needed for invagination of retina during optic cup formation. Dev Dyn. 2004 Oct;231(2):270-7. Pubmed
      2. Everts HB, King LE Jr, Sundberg JP, Ong DE: Hair cycle-specific immunolocalization of retinoic acid synthesizing enzymes Aldh1a2 and Aldh1a3 indicate complex regulation. J Invest Dermatol. 2004 Aug;123(2):258-63. Pubmed
      3. Gidlof AC, Ocaya P, Olofsson PS, Torma H, Sirsjo A: Differences in retinol metabolism and proliferative response between neointimal and medial smooth muscle cells. J Vasc Res. 2006;43(4):392-8. Epub 2006 Jul 6. Pubmed
      4. Matt N, Dupe V, Garnier JM, Dennefeld C, Chambon P, Mark M, Ghyselinck NB: Retinoic acid-dependent eye morphogenesis is orchestrated by neural crest cells. Development. 2005 Nov;132(21):4789-800. Epub 2005 Oct 5. Pubmed
      5. Kim H, Lapointe J, Kaygusuz G, Ong DE, Li C, van de Rijn M, Brooks JD, Pollack JR: The retinoic acid synthesis gene ALDH1a2 is a candidate tumor suppressor in prostate cancer. Cancer Res. 2005 Sep 15;65(18):8118-24. Pubmed

      5. Retinoic acid-induced protein 3

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Components

      Name UniProt ID Details
      Retinoic acid-induced protein 3 Q8NFJ5 Details

      References:

      1. Xu J, Tian J, Shapiro SD: Normal lung development in RAIG1-deficient mice despite unique lung epithelium-specific expression. Am J Respir Cell Mol Biol. 2005 May;32(5):381-7. Epub 2005 Jan 27. Pubmed
      2. Inoue S, Nambu T, Shimomura T: The RAIG family member, GPRC5D, is associated with hard-keratinized structures. J Invest Dermatol. 2004 Mar;122(3):565-73. Pubmed

      6. Nuclear receptor subfamily 0 group B member 1

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Components

      Name UniProt ID Details
      Nuclear receptor subfamily 0 group B member 1 P51843 Details

      References:

      1. Overington JP, Al-Lazikani B, Hopkins AL: How many drug targets are there? Nat Rev Drug Discov. 2006 Dec;5(12):993-6. Pubmed
      2. Imming P, Sinning C, Meyer A: Drugs, their targets and the nature and number of drug targets. Nat Rev Drug Discov. 2006 Oct;5(10):821-34. Pubmed

      7. Retinal dehydrogenase 2

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Components

      Name UniProt ID Details
      Retinal dehydrogenase 2 O94788 Details

      References:

      1. Mic FA, Sirbu IO, Duester G: Retinoic acid synthesis controlled by Raldh2 is required early for limb bud initiation and then later as a proximodistal signal during apical ectodermal ridge formation. J Biol Chem. 2004 Jun 18;279(25):26698-706. Epub 2004 Apr 6. Pubmed
      2. Bordelon T, Montegudo SK, Pakhomova S, Oldham ML, Newcomer ME: A disorder to order transition accompanies catalysis in retinaldehyde dehydrogenase type II. J Biol Chem. 2004 Oct 8;279(41):43085-91. Epub 2004 Aug 7. Pubmed
      3. Mic FA, Molotkov A, Molotkova N, Duester G: Raldh2 expression in optic vesicle generates a retinoic acid signal needed for invagination of retina during optic cup formation. Dev Dyn. 2004 Oct;231(2):270-7. Pubmed
      4. Doxakis E, Davies AM: Retinoic acid negatively regulates GDNF and neurturin receptor expression and responsiveness in embryonic chicken sympathetic neurons. Mol Cell Neurosci. 2005 Aug;29(4):617-27. Pubmed
      5. Everts HB, Sundberg JP, Ong DE: Immunolocalization of retinoic acid biosynthesis systems in selected sites in rat. Exp Cell Res. 2005 Aug 15;308(2):309-19. Pubmed

      8. Retinoic acid receptor responder protein 1

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: agonist

      Components

      Name UniProt ID Details
      Retinoic acid receptor responder protein 1 P49788 Details

      References:

      1. Youssef EM, Chen XQ, Higuchi E, Kondo Y, Garcia-Manero G, Lotan R, Issa JP: Hypermethylation and silencing of the putative tumor suppressor Tazarotene-induced gene 1 in human cancers. Cancer Res. 2004 Apr 1;64(7):2411-7. Pubmed
      2. Zirn B, Samans B, Spangenberg C, Graf N, Eilers M, Gessler M: All-trans retinoic acid treatment of Wilms tumor cells reverses expression of genes associated with high risk and relapse in vivo. Oncogene. 2005 Aug 4;24(33):5246-51. Pubmed

      1. Cytochrome P450 3A7

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: substrate

      Components

      Name UniProt ID Details
      Cytochrome P450 3A7 P24462 Details

      References:

      1. Marill J, Cresteil T, Lanotte M, Chabot GG: Identification of human cytochrome P450s involved in the formation of all-trans-retinoic acid principal metabolites. Mol Pharmacol. 2000 Dec;58(6):1341-8. Pubmed

      2. Cytochrome P450 2B6

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: substrate

      Components

      Name UniProt ID Details
      Cytochrome P450 2B6 P20813 Details

      References:

      1. Marill J, Cresteil T, Lanotte M, Chabot GG: Identification of human cytochrome P450s involved in the formation of all-trans-retinoic acid principal metabolites. Mol Pharmacol. 2000 Dec;58(6):1341-8. Pubmed

      3. Cytochrome P450 2C8

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: substrate

      Components

      Name UniProt ID Details
      Cytochrome P450 2C8 P10632 Details

      References:

      1. Marill J, Cresteil T, Lanotte M, Chabot GG: Identification of human cytochrome P450s involved in the formation of all-trans-retinoic acid principal metabolites. Mol Pharmacol. 2000 Dec;58(6):1341-8. Pubmed

      4. Cytochrome P450 2C9

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: substrate

      Components

      Name UniProt ID Details
      Cytochrome P450 2C9 P11712 Details

      References:

      1. Marill J, Cresteil T, Lanotte M, Chabot GG: Identification of human cytochrome P450s involved in the formation of all-trans-retinoic acid principal metabolites. Mol Pharmacol. 2000 Dec;58(6):1341-8. Pubmed

      5. Cytochrome P450 3A4

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: substrate

      Components

      Name UniProt ID Details
      Cytochrome P450 3A4 P08684 Details

      References:

      1. Marill J, Cresteil T, Lanotte M, Chabot GG: Identification of human cytochrome P450s involved in the formation of all-trans-retinoic acid principal metabolites. Mol Pharmacol. 2000 Dec;58(6):1341-8. Pubmed

      6. Cytochrome P450 3A5

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: substrate

      Components

      Name UniProt ID Details
      Cytochrome P450 3A5 P20815 Details

      References:

      1. Marill J, Cresteil T, Lanotte M, Chabot GG: Identification of human cytochrome P450s involved in the formation of all-trans-retinoic acid principal metabolites. Mol Pharmacol. 2000 Dec;58(6):1341-8. Pubmed

      7. Cytochrome P450 2A6

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: substrate

      Components

      Name UniProt ID Details
      Cytochrome P450 2A6 P11509 Details

      References:

      1. Marill J, Cresteil T, Lanotte M, Chabot GG: Identification of human cytochrome P450s involved in the formation of all-trans-retinoic acid principal metabolites. Mol Pharmacol. 2000 Dec;58(6):1341-8. Pubmed

      8. Cytochrome P450 2C18

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: substrate

      Components

      Name UniProt ID Details
      Cytochrome P450 2C18 P33260 Details

      References:

      1. Marill J, Cresteil T, Lanotte M, Chabot GG: Identification of human cytochrome P450s involved in the formation of all-trans-retinoic acid principal metabolites. Mol Pharmacol. 2000 Dec;58(6):1341-8. Pubmed

      9. Cytochrome P450 1A1

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: substrate

      Components

      Name UniProt ID Details
      Cytochrome P450 1A1 P04798 Details

      References:

      1. Marill J, Cresteil T, Lanotte M, Chabot GG: Identification of human cytochrome P450s involved in the formation of all-trans-retinoic acid principal metabolites. Mol Pharmacol. 2000 Dec;58(6):1341-8. Pubmed

      10. Cytochrome P450 4A11

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: substrate

      Components

      Name UniProt ID Details
      Cytochrome P450 4A11 Q02928 Details

      References:

      1. Marill J, Cresteil T, Lanotte M, Chabot GG: Identification of human cytochrome P450s involved in the formation of all-trans-retinoic acid principal metabolites. Mol Pharmacol. 2000 Dec;58(6):1341-8. Pubmed

      1. Cellular retinoic acid-binding protein 1

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: substrate

      Components

      Name UniProt ID Details
      Cellular retinoic acid-binding protein 1 P29762 Details

      References:

      1. Hoegberg P, Schmidt CK, Fletcher N, Nilsson CB, Trossvik C, Gerlienke Schuur A, Brouwer A, Nau H, Ghyselinck NB, Chambon P, Hakansson H: Retinoid status and responsiveness to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in mice lacking retinoid binding protein or retinoid receptor forms. Chem Biol Interact. 2005 Sep 10;156(1):25-39. Pubmed
      2. Donato LJ, Noy N: Fluorescence-based technique for analyzing retinoic acid. Methods Mol Biol. 2010;652:177-87. Pubmed

      2. Cellular retinoic acid-binding protein 2

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: substrate

      Components

      Name UniProt ID Details
      Cellular retinoic acid-binding protein 2 P29373 Details

      References:

      1. Hoegberg P, Schmidt CK, Fletcher N, Nilsson CB, Trossvik C, Gerlienke Schuur A, Brouwer A, Nau H, Ghyselinck NB, Chambon P, Hakansson H: Retinoid status and responsiveness to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in mice lacking retinoid binding protein or retinoid receptor forms. Chem Biol Interact. 2005 Sep 10;156(1):25-39. Pubmed
      2. Ohnishi K: PML-RARalpha inhibitors (ATRA, tamibaroten, arsenic troxide) for acute promyelocytic leukemia. Int J Clin Oncol. 2007 Oct;12(5):313-7. Epub 2007 Oct 22. Pubmed
      3. Donato LJ, Noy N: Fluorescence-based technique for analyzing retinoic acid. Methods Mol Biol. 2010;652:177-87. Pubmed

      Comments
      Drug created on June 13, 2005 07:24 / Updated on September 16, 2013 17:12