^ abcdefghijklmnopqrstuv“Bicalutamide: clinical pharmacokinetics and metabolism”. Clinical Pharmacokinetics43 (13): 855–878. (2004). doi:10.2165/00003088-200443130-00003. PMID15509184. "These data indicate that direct glucuronidation is the main metabolic pathway for the rapidly cleared (S)-bicalutamide, whereas hydroxylation followed by glucuronidation is a major metabolic pathway for the slowly cleared (R)-bicalutamide."
^ ab“Nilutamide: an antiandrogen for the treatment of prostate cancer”. The Annals of Pharmacotherapy31 (1): 65–75. (1997). doi:10.1177/106002809703100112. PMID8997470. "page 67: Currently, information is not available regarding the activity of the major urinary metabolites of bicalutamide, bicalutamide glucuronide, and hydroxybicalutamide glucuronide."
^ ab“An evaluation of bicalutamide in the treatment of prostate cancer”. Expert Opinion on Pharmacotherapy3 (9): 1313–28. (September 2002). doi:10.1517/14656566.3.9.1313. PMID12186624. "The clearance of bicalutamide occurs pre- dominantly by hepatic metabolism and glucuronidation, with excretion of the resulting inactive metabolites in the urine and faces."
^“Androgen deprivation therapy for prostate cancer: recommendations to improve patient and partner quality of life”. The Journal of Sexual Medicine7 (9): 2996–3010. (2010). doi:10.1111/j.1743-6109.2010.01902.x. PMID20626600.
^“Drug-induced photosensitivity to bicalutamide – case report and review of the literature”. Photodermatology, Photoimmunology & Photomedicine32 (3): 161–4. (May 2016). doi:10.1111/phpp.12230. PMID26663090.
^“Drug-induced photosensitivity to bicalutamide – case report and review of the literature”. Reactions Weekly1612 (1): 37. (2016). doi:10.1007/s40278-016-19790-1.
^“Clinical pharmacokinetics of the antiandrogens and their efficacy in prostate cancer”. Clinical Pharmacokinetics34 (5): 405–17. (May 1998). doi:10.2165/00003088-199834050-00005. PMID9592622.
^World Health Organization model list of essential medicines: 21st list 2019. Geneva: World Health Organization. (2019). WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO
^Hamilton, Richart (2015). Tarascon Pocket Pharmacopoeia 2015 Deluxe Lab-Coat Edition. Jones & Bartlett Learning. p. 381. ISBN9781284057560
^“Bicalutamide”. International Drug Price Indicator Guide. 8 December 2016閲覧。
^“[A new anti-androgen, bicalutamide (Casodex), for the treatment of prostate cancer—basic clinical aspects]” (Japanese). Gan to Kagaku Ryoho. Cancer & Chemotherapy26 (8): 1201–7. (1999). PMID10431591.
^Campbell (22 January 2014). “Slowing Sales for Johnson & Johnson's Zytiga May Be Good News for Medivation”. The Motley Fool. 26 August 2016時点のオリジナルよりアーカイブ。20 July 2016閲覧。 “[...] the most commonly prescribed treatment for metastatic castration resistant prostate cancer: bicalutamide. That was sold as AstraZeneca's billion-dollar-a-year drug Casodex before losing patent protection in 2008. AstraZeneca still generates a few hundred million dollars in sales from Casodex, [...]”
^ ab“Current topics and perspectives relating to hormone therapy for prostate cancer”. International Journal of Clinical Oncology13 (5): 401–10. (October 2008). doi:10.1007/s10147-008-0830-y. PMID18946750.
^ ab“Bicalutamide 80 mg combined with a luteinizing hormone-releasing hormone agonist (LHRH-A) versus LHRH-A monotherapy in advanced prostate cancer: findings from a phase III randomized, double-blind, multicenter trial in Japanese patients”. Prostate Cancer Prostatic Dis.10 (2): 194–201. (2007). doi:10.1038/sj.pcan.4500934. PMID17199134. "In most countries, bicalutamide is given at a dose of 50 mg when used in combination with an LHRH-A. However, based on pharmacokinetic and pharmacodynamic data, the approved dose of bicalutamide in Japanese men is 80 mg per day."
^“Clinical benefits of bicalutamide compared with flutamide in combined androgen blockade for patients with advanced prostatic carcinoma: final report of a double-blind, randomized, multicenter trial. Casodex Combination Study Group”. Urology50 (3): 330–6. (September 1997). doi:10.1016/S0090-4295(97)00279-3. PMID9301693.
^“Bicalutamide vs cyproterone acetate in preventing flare with LHRH analogue therapy for prostate cancer—a pilot study”. Prostate Cancer and Prostatic Diseases8 (1): 91–4. (2005). doi:10.1038/sj.pcan.4500784. PMID15711607.
^ abc“Update on idiopathic hirsutism: diagnosis and treatment”. Acta Clinica Belgica68 (4): 268–74. (2013). doi:10.2143/ACB.3267. PMID24455796.
^“Combined Oral Contraception and Bicalutamide in Polycystic Ovary Syndrome and Severe Hirsutism: A Double-Blind Randomized Controlled Trial”. J. Clin. Endocrinol. Metab.103 (3): 824–838. (March 2018). doi:10.1210/jc.2017-01186. PMID29211888.
^Gooren, LJ (31 March 2011). “Clinical practice. Care of transsexual persons.”. The New England Journal of Medicine364 (13): 1251–7. doi:10.1056/nejmcp1008161. PMID21449788.
^“Clinical review: Breast development in trans women receiving cross-sex hormones”. The Journal of Sexual Medicine11 (5): 1240–7. (May 2014). doi:10.1111/jsm.12487. PMID24618412.
^Haddad, Nadine G.; Eugster, Erica A. (2019). “Peripheral precocious puberty including congenital adrenal hyperplasia: causes, consequences, management and outcomes”. Best Practice & Research Clinical Endocrinology & Metabolism33 (3): 101273. doi:10.1016/j.beem.2019.04.007. hdl:1805/19111. ISSN1521-690X. PMID31027974.
^Haddad, Nadine G.; Eugster, Erica A. (2012). “Peripheral Precocious Puberty: Interventions to Improve Growth”. Handbook of Growth and Growth Monitoring in Health and Disease. pp. 1199–1212. doi:10.1007/978-1-4419-1795-9_71. ISBN978-1-4419-1794-2
^“Bicalutamide plus anastrozole for the treatment of gonadotropin-independent precocious puberty in boys with testotoxicosis: a phase II, open-label pilot study (BATT)”. Journal of Pediatric Endocrinology & Metabolism23 (10): 999–1009. (October 2010). doi:10.1515/jpem.2010.161. PMID21158211.
^“Clinical review: Ethical and medical considerations of androgen deprivation treatment of sex offenders”. The Journal of Clinical Endocrinology & Metabolism96 (12): 3628–37. (2011). doi:10.1210/jc.2011-1540. PMID21956411.
^“Potential side effects of androgen deprivation treatment in sex offenders”. The Journal of the American Academy of Psychiatry and the Law37 (1): 53–8. (2009). PMID19297634.
^“The efficacy, safety and ethics of the use of testosterone-suppressing agents in the management of sex offending”. Current Opinion in Endocrinology, Diabetes and Obesity23 (3): 271–8. (2016). doi:10.1097/MED.0000000000000257. PMID27032060.
^“Effect of combined androgen blockade with an LHRH agonist and flutamide in one severe case of male exhibitionism”. The Canadian Journal of Psychiatry35 (4): 338–41. (1990). doi:10.1177/070674379003500412. PMID2189544.
^ abcd“Nonsteroidal antiandrogens: a therapeutic option for patients with advanced prostate cancer who wish to retain sexual interest and function”. BJU International87 (1): 47–56. (January 2001). doi:10.1046/j.1464-410x.2001.00988.x. PMID11121992.
^“Hormone therapy of prostate cancer: is there a role for antiandrogen monotherapy?”. Crit. Rev. Oncol. Hematol.35 (2): 121–32. (2000). doi:10.1016/s1040-8428(00)00051-2. PMID10936469.
^“Hepatotoxicity induced by antiandrogens: a review of the literature”. Urol. Int.73 (4): 289–95. (2004). doi:10.1159/000081585. PMID15604569.
^“Pneumonitis associated with nonsteroidal antiandrogens: presumptive evidence of a class effect”. Annals of Internal Medicine137 (7): 625. (October 2002). doi:10.7326/0003-4819-137-7-200210010-00029. PMID12353966. "An estimated 0.77% of the 6,480 nilutamide-treated patients, 0.04% of the 41,700 flutamide-treated patients, and 0.01% of the 86,800 bicalutamide-treated patients developed pneumonitis during the study period."
^“Drug safety is a barrier to the discovery and development of new androgen receptor antagonists”. Prostate71 (5): 480–8. (2011). doi:10.1002/pros.21263. PMID20878947.
^“Enzalutamide: a review of its use in chemotherapy-naïve metastatic castration-resistant prostate cancer”. Drugs Aging32 (3): 243–9. (2015). doi:10.1007/s40266-015-0248-y. PMID25711765.
^“The preclinical development of bicalutamide: pharmacodynamics and mechanism of action”. Urology47 (1A Suppl): 13–25; discussion 29–32. (1996). doi:10.1016/S0090-4295(96)80003-3. PMID8560673.
^“Adverse reactions to spironolactone. A report from the Boston Collaborative Drug Surveillance Program”. JAMA225 (1): 40–3. (July 1973). doi:10.1001/jama.1973.03220280028007. PMID4740303.
^“Serum C-reactive protein (CRP) levels and insulin resistance in non-obese women with polycystic ovarian syndrome, and effect of bicalutamide on hirsutism, CRP levels and insulin resistance”. Hormone Research62 (6): 283–7. (2004). doi:10.1159/000081973. PMID15542929.
^ ab“Tolerability, efficacy and pharmacokinetics of bicalutamide 300 mg, 450 mg or 600 mg as monotherapy for patients with locally advanced or metastatic prostate cancer, compared with castration”. BJU International98 (3): 563–72. (September 2006). doi:10.1111/j.1464-410X.2006.06275.x. PMID16771791.
^Genrx (1999). 1999 Mosby's GenRx. Mosby. ISBN978-0-323-00625-5. https://books.google.com/books?id=Td6ZFsVsCswC. "A 79-year-old man attempted suicide by ingesting 13g of nilutamide (i.e., 43 times the maximum recommended dose). Despite immediate gastric lavage and oral administration of activated charcoal, plasma nilutamide levels peaked at 6 times the normal range 2 hours after ingestion. There were no clinical signs or symptoms or changes in parameters such as transaminases or chest x-ray. Maintenance treatment (150 mg/day) was resumed 30 days later."
^“Bicalutamide functions as an androgen receptor antagonist by assembly of a transcriptionally inactive receptor”. The Journal of Biological Chemistry277 (29): 26321–6. (July 2002). doi:10.1074/jbc.M203310200. PMID12015321.
^“Testosterone/bicalutamide antagonism at the predicted extracellular androgen binding site of ZIP9”. Biochim. Biophys. Acta1864 (12): 2402–2414. (2017). doi:10.1016/j.bbamcr.2017.09.012. PMID28943399.
^ abc“Clinical pharmacokinetics of the antiandrogens and their efficacy in prostate cancer”. Clinical Pharmacokinetics34 (5): 405–17. (May 1998). doi:10.2165/00003088-199834050-00005. PMID9592622.
^“Effects on the endocrine system of long-term treatment with the non-steroidal anti-androgen Casodex in patients with benign prostatic hyperplasia”. British Journal of Urology75 (3): 335–40. (March 1995). doi:10.1111/j.1464-410X.1995.tb07345.x. PMID7537602.
^ abBouchard, P.; Caraty, A. (15 November 1993). GnRH, GnRH Analogs, Gonadotropins and Gonadal Peptides. CRC Press. pp. 455–456. ISBN978-0-203-09205-7. https://books.google.com/books?id=uctURfWwTb4C&pg=PA455. "[...] when male levels of androgens are achieved in plasma, their effects on gonadotropin secretion are similar in women and men. [...] administration of flutamide in a group of normally-cycling women produced a clinical improvement of acne and hirsutism without any significant hormonal change. [...] All these data emphasize that physiological levels of androgens have no action on the regulation of gonadotropins in normal women. [...] Androgens do not directly play a role in gonadotropin regulation [in women]."
^Shlomo Melmed (1 January 2016). Williams Textbook of Endocrinology. Elsevier Health Sciences. pp. 752–. ISBN978-0-323-29738-7. https://books.google.com/books?id=YZ8_CwAAQBAJ&pg=PA752. "GnRH analogues, both agonists and antagonists, severely suppress endogenous gonadotropin and testosterone production [...] Administration of GnRH agonists (e.g., leuprolide, goserelin) produces an initial stimulation of gonadotropin and testosterone secretion (known as a "flare"), which is followed in 1 to 2 weeks by GnRH receptor downregulation and marked suppression of gonadotropins and testosterone to castration levels. [...] To prevent the potential complications associated with the testosterone flare, AR antagonists (e.g., bicalutamide) are usually coadministered with a GnRH agonist for men with metastatic prostate cancer.399"
^“Reduction in undesired sexual hair growth with anandron in male-to-female transsexuals—experiences with a novel androgen receptor blocker”. Clinical and Experimental Dermatology14 (5): 361–3. (1989). doi:10.1111/j.1365-2230.1989.tb02585.x. PMID2612040.
^ ab“Role of estrogen in normal male function: clinical implications for patients with prostate cancer on androgen deprivation therapy”. The Journal of Urology185 (1): 17–23. (January 2011). doi:10.1016/j.juro.2010.08.094. PMID21074215.
^ ab“Preliminary study with bicalutamide in heterosexual and homosexual patients with prostate cancer: a possible implication of androgens in male homosexual arousal”. BJU International108 (1): 110–5. (July 2011). doi:10.1111/j.1464-410X.2010.09764.x. PMID20955264.
^ ab“The effect of estrogen on the sexual interest of castrated males: Implications to prostate cancer patients on androgen-deprivation therapy”. Critical Reviews in Oncology/Hematology87 (3): 224–38. (September 2013). doi:10.1016/j.critrevonc.2013.01.006. PMID23484454.
^“Mechanisms regulating male sexual behavior in the rat: role of 3 alpha- and 3 beta-androstanediols”. Biology of Reproduction51 (3): 562–71. (September 1994). doi:10.1095/biolreprod51.3.562. PMID7803627.
^“An estrogenic effect of 5alpha-androstane-3beta, 17beta-diol on the behavioral response to stress and on CRH regulation”. Neuropharmacology54 (8): 1233–8. (June 2008). doi:10.1016/j.neuropharm.2008.03.016. PMID18457850.
^“Effects of long-term treatment with the anti-androgen bicalutamide on human testis: an ultrastructural and morphometric study”. Histopathology38 (3): 195–201. (March 2001). doi:10.1046/j.1365-2559.2001.01077.x. PMID11260298.
^ abJones, C. A.; Reiter, L.; Greenblatt, E. (2016). “Fertility preservation in transgender patients”. International Journal of Transgenderism17 (2): 76–82. doi:10.1080/15532739.2016.1153992. ISSN1553-2739. "Traditionally, patients have been advised to cryopreserve sperm prior to starting cross-sex hormone therapy as there is a potential for a decline in sperm motility with high-dose estrogen therapy over time (Lubbert et al., 1992). However, this decline in fertility due to estrogen therapy is controversial due to limited studies."
^ abPayne, Anita H.; Hardy, Matthew P. (28 October 2007). The Leydig Cell in Health and Disease. Springer Science & Business Media. pp. 422–431. ISBN978-1-59745-453-7. https://books.google.com/books?id=x4ttqKIAOg0C&pg=PA422. "Estrogens are highly efficient inhibitors of the hypothalamic-hypophyseal-testicular axis (212–214). Aside from their negative feedback action at the level of the hypothalamus and pituitary, direct inhibitory effects on the testis are likely (215,216). [...] The histology of the testes [with estrogen treatment] showed disorganization of the seminiferous tubules, vacuolization and absence of lumen, and compartmentalization of spermatogenesis."
^ ab“The antiandrogen cyproterone acetate: discovery, chemistry, basic pharmacology, clinical use and tool in basic research”. Exp. Clin. Endocrinol.102 (1): 1–32. (1994). doi:10.1055/s-0029-1211261. PMID8005205. "Spermatogenesis is also androgen-dependent and is inhibited by CPA, meaning that patients treated with high doses of CPA are sterile (Figure 23). All the effects of CPA are fully reversible."
^ abSalam, Muhammad A. (2003). Principles & Practice of Urology: A Comprehensive Text. Universal-Publishers. pp. 684–. ISBN978-1-58112-412-5. https://books.google.com/books?id=y50kTcCCfEcC&pg=PA684. "Estrogens act primarily through negative feedback at the hypothalamic-pituitary level to reduce LH secretion and testicular androgen synthesis. [...] Interestingly, if the treatment with estrogens is discontinued after 3 yr. of uninterrupted exposure, serum testosterone may remain at castration levels for up to another 3 yr. This prolonged suppression is thought to result from a direct effect of estrogens on the Leydig cells."
^ ab“Drug safety is a barrier to the discovery and development of new androgen receptor antagonists”. The Prostate71 (5): 480–8. (April 2011). doi:10.1002/pros.21263. PMID20878947.
^ abcdefgWeber, Georg F. (22 July 2015). Molecular Therapies of Cancer. Springer. pp. 318–. ISBN978-3-319-13278-5. https://books.google.com/books?id=dhs_CgAAQBAJ&pg=PA318. "Compared to flutamide and nilutamide, bicalutamide has a 2-fold increased affinity for the Androgen Receptor, a longer half-life, and substantially reduced toxicities. Based on a more favorable safety profile relative to flutamide, bicalutamide is indicated for use in combination therapy with a Gonadotropin Releasing Hormone analog for the treatment of advanced metastatic prostate carcinoma."
^“Tolerability, efficacy and pharmacokinetics of bicalutamide 300 mg, 450 mg or 600 mg as monotherapy for patients with locally advanced or metastatic prostate cancer, compared with castration”. BJU International98 (3): 563–72. (September 2006). doi:10.1111/j.1464-410X.2006.06275.x. PMID16771791.
^“Clinical progress with a new antiandrogen, Casodex (bicalutamide)”. Eur. Urol.29 Suppl 2: 96–104. (1996). doi:10.1159/000473847. PMID8717470.
^“ICI 176,334: a novel non-steroidal, peripherally selective antiandrogen”. The Journal of Endocrinology113 (3): R7-9. (June 1987). doi:10.1677/joe.0.113R007. PMID3625091.
^“Bicalutamide in the treatment of advanced prostatic carcinoma: a phase II noncomparative multicenter trial evaluating safety, efficacy and long-term endocrine effects of monotherapy”. The Journal of Urology154 (6): 2110–4. (December 1995). doi:10.1016/S0022-5347(01)66709-0. PMID7500470.
^“What implications do the tolerability profiles of antiandrogens and other commonly used prostate cancer treatments have on patient care?”. Journal of Cancer Research and Clinical Oncology132 Suppl 1: S27-35. (August 2006). doi:10.1007/s00432-006-0134-4. PMID16896883.
^“Bicalutamide (Casodex) in the treatment of prostate cancer”. Expert Review of Anticancer Therapy4 (1): 37–48. (February 2004). doi:10.1586/14737140.4.1.37. PMID14748655. "In contrast, the incidence of diarrhea was comparable between the bicalutamide and placebo groups (6.3 vs. 6.4%, respectively) in the EPC program [71]."
^“Development and validation of a highly sensitive LC-MS/MS-ESI method for the determination of bicalutamide in mouse plasma: application to a pharmacokinetic study”. Biomedical Chromatography26 (12): 1589–95. (2012). doi:10.1002/bmc.2736. PMID22495777.
^Anderson, Philip O.; Knoben, James E.; Troutman, William G. (22 August 2001). Handbook of Clinical Drug Data. 128. McGraw Hill Professional. 245. ISBN978-0-07-138942-6. PMC1875767. PMID20313924. https://books.google.com/books?id=40UJmr_6WQ4C. "With an oral dose of 50 mg/day, bicalutamide attains a peak serum level of 8.9 mg/L (21 μmol/L) 31 hr after a dose at steady state. CI of (R)-bicalutamide is 0.32 L/hr. The active (R)-enantiomer of bicalutamide is oxidized to an inactive metabolite, which, like the inactive (S)-enantiomer, is glucuronidated and cleared rapidly by elimination in the urine and feces.165"
^ ab“Nonsteroidal selective androgen receptor modulators (SARMs): dissociating the anabolic and androgenic activities of the androgen receptor for therapeutic benefit”. Journal of Medicinal Chemistry52 (12): 3597–617. (June 2009). doi:10.1021/jm900280m. PMID19432422.
^“The response of advanced prostatic cancer to a new non-steroidal antiandrogen: results of a multicenter open phase II study of Casodex. European/Australian Co-operative Group”. European Urology18 Suppl 3: 18–21. (1990). doi:10.1159/000463973. PMID2094607.
^Bono, Aldo V (2004). “Overview of Current Treatment Strategies in Prostate Cancer”. European Urology Supplements3 (1): 2–7. doi:10.1016/j.eursup.2003.12.002. "The Canadian Health Authorities have withdrawn the approval for antiandrogen monotherapy with bicalutamide for the treatment of localised prostate cancer [5]. Several European countries have also withdrawn approval for bicalutamide for this indication."
^Nargund, Vinod H.; Raghavan, Derek; Sandler, Howard M. (17 January 2015). Urological Oncology. Springer. pp. 823–. ISBN978-0-85729-482-1. https://books.google.com/books?id=WmgzBgAAQBAJ&pg=PA823. "On the other hand, the 150 mg dose of bicalutamide has been associated with some safety concerns, such as a higher death rate when added to active surveillance in the early prostate cancer trialists group study [29], which has led the United States and Canada to recommend against prescribing the 150 mg dose [30]."