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药品详细

Tretinoin(维甲酸)

化学结构式图
中文名
维甲酸
英文名
Tretinoin
分子式
C20H28O2
化学名
3,7-dimethyl-9-(2,6,6-trimethylcyclohex-1-en-1-yl)nona-2,4,6,8-tetraenoic acid
分子量
Average: 300.4351
Monoisotopic: 300.20893014
CAS号
302-79-4
ATC分类
D10A Anti-Acne Preparations for Topical Use;D10A Anti-Acne Preparations for Topical Use;L01X 其它抗肿瘤药;D10B 未知;D10A Anti-Acne Preparations for Topical Use;L01X 其它抗肿瘤药
药物类型
small molecule
阶段
approved, nutraceutical
商品名
同义名
基本介绍

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).

生产厂家
  • Barr laboratories inc
  • Dow pharmaceutical sciences inc
  • Genpharm inc
  • Hoffmann la roche inc
  • Johnson and johnson consumer companies inc
  • Mylan bertek pharmaceuticals inc
  • Mylan pharmaceuticals inc
  • Ortho dermatologics
  • Ranbaxy laboratories ltd
  • Ranbaxy pharmaceuticals inc
  • Ranbaxy Pharmaceuticals Inc.
  • Spear pharmaceuticals inc
  • Teva pharmaceuticals usa
  • Triax pharmaceuticals llc
  • Wockhardt eu operations (swiss) ag
封装厂家
参考
Synthesis Reference Not 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
剂型
规格
化合物类型
Type small molecule
Classes
  • Retinoids
Substructures
  • Hydroxy Compounds
  • Alkanes and Alkenes
  • Retinoids
  • Acetates
  • Carboxylic Acids and Derivatives
  • Monoterpenes
  • Isoprenes
  • Cyclohexenes and Derivatives
适应症
药理
Indication 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.
Pharmacodynamics 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).
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.
Absorption 1-31% (topical)
Volume of distribution Not Available
Protein binding > 95%
Metabolism
Hepatic

Important The metabolism module of DrugBank is currently in beta. Questions or suggestions? Please contact us.

Substrate Enzymes Product
Tretinoin
4-Hydroxyretinoic acid Details
Tretinoin
18-Hydroxyretinoic acid Details
Tretinoin
5,6-Epoxyretinoic acid Details
Tretinoin
4-Oxoretinoic acid Details
Tretinoin
    		Retinoyl b-glucuronide Details
    Tretinoin
      		Retinyl beta-glucuronide Details
      Route of elimination Not Available
      Half life 0.5-2 hours
      Clearance Not Available
      Toxicity Not Available
      Affected organisms
      • Humans and other mammals
      Pathways Not Available
      理化性质
      Properties
      State solid
      Experimental Properties
      Property Value Source
      melting point 181 °C PhysProp
      water solubility <0.1 g/100 mL Not Available
      logP 6.30 HANSCH,C ET AL. (1995)
      Predicted Properties
      Property Value Source
      water solubility 4.77e-03 g/l ALOGPS
      logP 5.66 ALOGPS
      logP 5.01 ChemAxon
      logS -4.8 ALOGPS
      pKa (strongest acidic) 5 ChemAxon
      physiological charge -1 ChemAxon
      hydrogen acceptor count 2 ChemAxon
      hydrogen donor count 1 ChemAxon
      polar surface area 37.3 ChemAxon
      rotatable bond count 5 ChemAxon
      refractivity 97.79 ChemAxon
      polarizability 36.62 ChemAxon
      药物相互作用
      Drug Interaction
      Atazanavir The 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.
      Carbamazepine The 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.
      Celecoxib The 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.
      Demeclocycline Demeclocycline may increase the adverse effects of oral Tretinoin. Increased risk of pseudotumour cerebri. Concurrent therapy should be avoided.
      Desogestrel Oral Tretinoin may decrease the effect of oral contraceptive, Desogestrel. An alternate form of contraception should be used during concomitant therapy.
      Doxycycline Doxycycline may increase the adverse effects of oral Tretinoin. Increase risk of pseudotumour cerebri. Concurrent therapy should be avoided.
      Drospirenone Oral Tretinoin may decrease the effect of oral contraceptive, Drospirenone. An alternate form of contraception should be used during concomitant therapy.
      Eltrombopag The 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 Estradiol Oral Tretinoin may decrease the effect of the oral contraceptive, Ethinyl Estradiol. An alternate form of contraception should be used during concomitant therapy.
      Ethynodiol Diacetate Oral Tretinoin may decrease the effect of oral contraceptive, Ethynodiol Diacetate. An alternate form of contraception should be used during concomitant therapy.
      Etonogestrel Oral Tretinoin may decrease the effect of oral contraceptive, Etonogestrel. An alternate form of contraception should be used during concomitant therapy.
      Felodipine The 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.
      Fosphenytoin The 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.
      Gemfibrozil The 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.
      Irbesartan The 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.
      Lapatinib The 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.
      Levonorgestrel Oral Tretinoin may decrease the effect of oral contraceptive, Levonorgestrel. An alternate form of contraception should be used during concomitant therapy.
      Losartan The 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.
      Mestranol Oral Tretinoin may decrease the effect of oral contraceptive, Mestranol. An alternate form of contraception should be used during concomitant therapy.
      Minocycline Minocycline may increase the adverse effects of oral Tretinoin. Increase risk of pseudotumour cerebri. Concurrent therapy should be avoided.
      Natalizumab Oral tretinoin may increase the adverse/toxic effects of Natalizumab. Concurrent therapy should be avoided.
      Nilotinib The 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.
      Norethindrone Oral Tretinoin may decrease the effect of oral contraceptive, Norethindrone. An alternate form of contraception should be used during concomitant therapy.
      Norgestimate Oral Tretinoin may decrease the effect of oral contraceptive, Norgestimate. An alternate form of contraception should be used during concomitant therapy.
      Oxytetracycline Oxytetracycline may increase the adverse effects of oral Tretinoin. Increase risk of pseudotumour cerebri. Concurrent therapy should be avoided.
      Phenobarbital The 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.
      Phenytoin The 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.
      Pioglitazone The 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.
      Primidone The 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.
      Quinine The 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.
      Rabeprazole The 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.
      Rifampin The 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.
      Rifapentine The 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.
      Ritonavir The 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.
      Rosiglitazone The 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.
      Secobarbital The 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.
      Sorafenib The 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.
      Tamoxifen The 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.
      Tetracycline Demeclocycline may increase the adverse effects of oral Tretinoin. Increase risk of pseudotumour cerebri. Concurrent therapy should be avoided.
      Tigecycline Demeclocycline may increase the adverse effects of oral Tretinoin. Increase risk of pseudotumour cerebri. Concurrent therapy should be avoided.
      Trastuzumab Increased risk of leukopenia and anemia due to synergistic effects. Monitor for signs and symptoms of adverse events during concomitant therapy.
      Trimethoprim The 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 A Tretinoin increases the risk of vitamin A toxicity. Avoid vitamin A supplementation while taking systemic tretinoin.
      食物相互作用
      Not Available

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