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the writing point of a pen (同)pen nib

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ペン先 / (一般的に)とがった部分,先端(tip) / (鳥の)くちばし

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/09/05 07:42:22」(JST)

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Gefitinib (INN, /ɡɛˈfɪtɨnɪb/, trade name Iressa, marketed by AstraZeneca and Teva), is a drug used for certain breast, lung and other cancers. Gefitinib is an EGFR inhibitor, like erlotinib, which interrupts signaling through the epidermal growth factor receptor (EGFR) in target cells. Therefore, it is only effective in cancers with mutated and overactive EGFR.

Mechanism of action

Gefitinib is the first selective inhibitor of epidermal growth factor receptor's (EGFR) tyrosine kinase domain. Thus gefitinib is an EGFR inhibitor. The target protein (EGFR) is a family of receptors which includes Her1(erb-B1), Her2(erb-B2), and Her 3(erb-B3). EGFR is overexpressed in the cells of certain types of human carcinomas - for example in lung and breast cancers. This leads to inappropriate activation of the anti-apoptotic Ras signalling cascade, eventually leading to uncontrolled cell proliferation. Research on gefitinib-sensitive non-small cell lung cancers has shown that a mutation in the EGFR tyrosine kinase domain is responsible for activating anti-apoptotic pathways.^[1]^[2] These mutations tend to confer increased sensitivity to tyrosine kinase inhibitors such as gefitinib and erlotinib. Of the types of non-small cell lung cancer histologies, adenocarcinoma is the type that most often harbors these mutations. These mutations are more commonly seen in Asians, women, and non-smokers (who also tend to more often have adenocarcinoma).

Gefitinib inhibits EGFR tyrosine kinase by binding to the adenosine triphosphate (ATP)-binding site of the enzyme. Thus the function of the EGFR tyrosine kinase in activating the anti-apoptotic Ras signal transduction cascade is inhibited, and malignant cells are inhibited.^[3]

Clinical uses

FDA approved in May 2003 for NSCLC,^[4] Gefitinib is currently marketed in over 64 countries.

In June 2005 the FDA withdrew approval for use in new patients due to lack of evidence that it extended life.^[5]

In Europe gefitinib is indicated since 2009 in advanced NSCLC in all lines of treatment for patients harbouring EGFR mutations. This label was granted after gefitinib demonstrated as a first line treatment to significantly improve progression-free survival vs. a platinum doublet regime in patients harbouring such mutations. IPASS has been the first of four phase III trials to have confirmed gefitinib superiority in this patient population.^{[citation needed]}

In most of the other countries where gefitinib is currently marketed it is approved for patients with advanced NSCLC who had received at least one previous chemotherapy regime. However, applications to expand its label as a first line treatment in patients harbouring EGFR mutations is currently in process based on the latest scientific evidence.^{[citation needed]} As at August 2012 New Zealand has approved gefitinib as first line treatment for patients with EGFR mutation for naive locally advanced or metastatic, unresectable NSCLC. This publicly funded for an initial 4 month term and renewal if no progression. ^[6]

While gefitinib has yet to be proven to be effective in other cancers, there is potential for its use in the treatment of other cancers where EGFR overexpression is involved.^{[citation needed]}

(Erlotinib is another EGFR tyrosine kinase inhibitor that has a similar mechanism of action to gefitinib.)

Experimental Uses

In August 2013, the BBC reported that researchers in Edinburgh and Melbourne found, in a small-scale trial of 12 patients, that the effectiveness of Methotrexate for treating ectopic pregnancy was improved when Gefitinib was also administered.^[7]

Studies

IPASS (IRESSA Pan-Asia Study) was a randomized, large-scale, double-blinded study which compared Gefitinib vs. carboplatin/ paclitaxel as a first line treatment in advanced NSCLC.^[8] IPASS studied 1,217 patients with confirmed adenocarcinoma histology who were former or never smokers. A pre-planned sub-group analyses showed that progression-free survival (PFS) was significantly longer for Gefitinib than chemotherapy in patients with EGFR mutation positive tumours (HR 0.48, 95 per cent CI 0.36 to 0.64, p less than 0.0001), and significantly longer for chemotherapy than Gefitinib in patients with EGFR mutation negative tumours (HR 2.85, 95 per cent CI 2.05 to 3.98, p less than 0.0001). This, in 2009, was the first time a targeted monotherapy has demonstrated significantly longer PFS than doublet chemotherapy.

EGFR Diagnostic tests

Genzyme, QIAGEN & other companies make tests to detect EGFR mutations, designed to help predict which lung cancer patients may respond best to some therapies, including Gefitinib and Erlotinib.

The tests examine the genetics of tumors removed for biopsy for mutations that make them susceptible to treatment.

The EGFR mutation test may also help AstraZeneca win regulatory approval for use of their drugs as initial therapies. Currently the TK inhibitors are approved for use only after other drugs fail.^{[citation needed]} In the case of gefitinib, the drug works only in about 10% of patients with advanced non-small cell lung cancer, the most common type of lung cancer.

Adverse effects

As gefitinib is a selective chemotherapeutic agent, its tolerability profile is better than previous cytotoxic agents. Adverse drug reactions (ADRs) are acceptable for a potentially fatal disease.

Acne-like rash is reported very commonly. Other common adverse effects (≥1% of patients) include: diarrhoea, nausea, vomiting, anorexia, stomatitis, dehydration, skin reactions, paronychia, asymptomatic elevations of liver enzymes, asthenia, conjunctivitis, blepharitis.^[9]

Infrequent adverse effects (0.1–1% of patients) include: interstitial lung disease, corneal erosion, aberrant eyelash and hair growth.^[9]

Iressa was approved and marketed from July 2002 in Japan, making it the first country to import the drug.

References

^ Pao W, Miller V, Zakowski M, et al. (September 2004). "EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib". Proceedings of the National Academy of Sciences of the United States of America 101 (36): 13306–11. doi:10.1073/pnas.0405220101. PMC 516528. PMID 15329413. Retrieved 2009-07-02.
^ Sordella R, Bell DW, Haber DA, Settleman J (August 2004). "Gefitinib-sensitizing EGFR mutations in lung cancer activate anti-apoptotic pathways". Science 305 (5687): 1163–7. doi:10.1126/science.1101637. PMID 15284455. |accessdate= requires |url= (help)
^ Takimoto CH, Calvo E. "Principles of Oncologic Pharmacotherapy" in Pazdur R, Wagman LD, Camphausen KA, Hoskins WJ (Eds) Cancer Management: A Multidisciplinary Approach. 11 ed. 2008.
^ http://www.accessdata.fda.gov/drugsatfda_docs/label/2003/021399lbl.pdf
^ http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm110473.htm
^ http://www.pharmac.govt.nz/2012/07/09/2012.07.10%20gefitinib%20funded.pdf
^ http://www.bbc.co.uk/news/uk-scotland-edinburgh-east-fife-24021956
^ Mok TS et al. Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma. N Eng J Med 2009; 361. 10.1056/NEJMoa0810699.
^ ^a ^b Rossi S, editor. Australian Medicines Handbook 2004. Adelaide: Australian Medicines Handbook; 2004. ISBN 0-9578521-4-2.

UpToDate Contents

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1. 進行非小細胞肺癌の治療歴がある患者に対するセカンドライン療法 second line therapy for patients with previously treated advanced non small cell lung cancer
2. 上皮成長因子受容体変異を有する進行性非小細胞肺癌に対する初期全身療法 initial systemic therapy for advanced non small cell lung cancer with a mutation in the epidermal growth factor receptor
3. 抗腫瘍療法関連肺毒性：分子標的剤 pulmonary toxicity associated with antineoplastic therapy molecularly targeted agents
4. 分子標的剤およびその他の生物製剤を用いた癌治療による皮膚合併症 cutaneous complications of molecularly targeted therapy and other biologic agents used for cancer therapy
5. 転移性膀胱癌の実験的全身療法 experimental systemic therapy of metastatic bladder cancer

English Journal

Gambogenic acid induces G1 arrest via GSK3β-dependent cyclin D1 degradation and triggers autophagy in lung cancer cells.

Yu XJ, Han QB, Wen ZS, Ma L, Gao J, Zhou GB.SourceDivision of Molecular Carcinogenesis and Targeted Therapy for Cancer, State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China; School of Life Sciences, University of Science and Technology of China, Hefei 230026, China.
Cancer letters.Cancer Lett.2012 Sep 28;322(2):185-94. Epub 2012 Mar 9.
Cyclin D1, an oncogenic G1 cyclin which can be induced by environmental carcinogens and whose over-expression may cause dysplasia and carcinoma, has been shown to be a target for cancer chemoprevention and therapy. In this study, we investigated the effects and underlying mechanisms of action of a p
PMID 22410463

A transformation in the mechanism by which the urokinase receptor signals provides a selection advantage for estrogen receptor-expressing breast cancer cells in the absence of estrogen.

Eastman BM, Jo M, Webb DL, Takimoto S, Gonias SL.AbstractBinding of urokinase-type plasminogen activator (uPA) to its receptor, uPAR, in estrogen receptor-α (ERα) expressing breast cancer cells, transiently activates ERK downstream of FAK, Src family kinases, and H-Ras. Herein, we show that when uPAR is over-expressed, in two separate ERα-positive breast cancer cell lines, ERK activation occurs autonomously of uPA and is sustained. Autonomous ERK activation by uPAR requires H-Ras and Rac1. A mutated form of uPAR, which does not bind vitronectin (uPAR-W32A), failed to induce autonomous ERK activation. Expression of human uPAR or mouse uPAR but not uPAR-W32A in MCF-7 cells provided a selection advantage when these cells were deprived of estrogen in cell culture for two weeks. Similarly, MCF-7 cells that express mouse uPAR formed xenografts in SCID mice that survived and increased in volume in the absence of estrogen supplementation, probably reflecting the pro-survival activity of phospho-ERK. Autonomous uPAR signaling to ERK was sensitive to the EGFR tyrosine kinase inhibitors, Erlotinib and Gefitinib. The transition in uPAR signaling from uPA-dependent and transient to autonomous and sustained is reminiscent of the transformation in ErbB2/HER2 signaling observed when this gene is amplified in breast cancer. uPAR over-expression may provide a pathway for escape of breast cancer cells from ERα-targeting therapeutics.
Cellular signalling.Cell Signal.2012 Sep;24(9):1847-55. Epub 2012 May 19.
Binding of urokinase-type plasminogen activator (uPA) to its receptor, uPAR, in estrogen receptor-α (ERα) expressing breast cancer cells, transiently activates ERK downstream of FAK, Src family kinases, and H-Ras. Herein, we show that when uPAR is over-expressed, in two separate ERα-positive brea
PMID 22617030

Japanese Journal

Comparison of Adverse Events of Erlotinib with those of Gefitinib in Patients with Non-small Cell Lung Cancer : A Case-control Study in Japansese Population

Suzumura Tomohiro,Kimura Tatsuo,Kudoh Shinzoh,Umekawa Kanako,Nagata Misato,Tanaka Hidenori,Mitsuoka Shigeki,Yoshimura Naruo,Kira Yukimi,Hirata Kazuto
Osaka City Medical journal 58(1), 25-34, 2012-06
NAID 110009418529

Met Kinase Inhibitor E7050 Reverses Three Different Mechanisms of Hepatocyte Growth Factor-induced Tyrosine Kinase Inhibitor Resistance in EGFR Mutant Lung Cancer

Wang Wei,Li Qi,Takeuchi Shinji,Yamada Tadaaki,Koizumi Hitomi,Nakamura Takahiro,Matsumoto Kunio,Mukaida Naofumi,Nishioka Yasuhiko,Sone Saburo,Nakagawa Takayuki,Uenaka Toshimitsu,Yano Seiji
Clinical Cancer Research 18(6), 1663-1671, 2012-03-15
… We assayed whether a new Met kinase inhibitor, E7050, which is currently being evaluated in clinical trials, could overcome these three mechanisms of resistance to EGFR-TKIs.EXPERIMENTAL DESIGN: The effects of E7050 on HGF-induced resistance to reversible (gefitinib), irreversible (BIBW2992), and mutant-selective (WZ4002) EGFR-TKIs were determined using the EGFR-mutant human lung cancer cell lines PC-9 and HCC827 with an exon 19 deletion, and H1975 with an T790M secondary mutation. …
NAID 120003830985

Related Pictures

★リンクテーブル★

リンク元	「ゲフィチニブ」「nib」「上皮成長因子受容体阻害薬」

「ゲフィチニブ」

Gefitinib
Systematic (IUPAC) name
	N-(3-chloro-4-fluoro-phenyl)-7-methoxy-; 6-(3-morpholin-4-ylpropoxy)quinazolin-4-amine
Clinical data
Trade names	Iressa
AHFS/Drugs.com	monograph
MedlinePlus	a607002
Pregnancy cat.	C (Au), D (U.S.)
Legal status	S4 (Au), POM (UK), ℞-only (U.S.)
Routes	Oral
Pharmacokinetic data
Bioavailability	59% (oral)
Protein binding	90%
Metabolism	Hepatic (mainly CYP3A4)
Half-life	6–49 hours
Excretion	Faecal
Identifiers
CAS number	184475-35-2
ATC code	L01XE02
PubChem	CID 123631
DrugBank	DB00317
ChemSpider	110217
UNII	S65743JHBS
KEGG	D01977
ChEBI	CHEBI:49668
ChEMBL	CHEMBL939
Chemical data
Formula	C22H24ClFN4O3
Mol. mass	446.902 g/mol
	SMILES COc1cc2c(cc1OCCCN3CCOCC3)c(ncn2)Nc4ccc(c(c4)Cl)F;
	InChI InChI=1S/C22H24ClFN4O3/c1-29-20-13-19-16(12-21(20)31-8-2-5-28-6-9-30-10-7-28)22(26-14-25-19)27-15-3-4-18(24)17(23)11-15/h3-4,11-14H,2,5-10H2,1H3,(H,25,26,27) ; Key:XGALLCVXEZPNRQ-UHFFFAOYSA-N ;
(what is this?) (verify)

　　[★]

英: gefitinib
商: イレッサ
関: 分子標的薬剤

分類

抗腫瘍薬

その他

チロシンキナーゼ阻害薬

特徴

構造

作用機序

EGF受容体チロシンキナーゼ(EGFR)のATP結合部位に競合的に結合する

ゲフィチニブの関連性の高いチロシンキナーゼであるHER2(Erb2/neu)に対する阻害活性は1/100と低い

セリン/スレオニンキナーゼに対する阻害作用なし

イレッサ錠250

ゲフィチニブは上皮成長因子受容体（EGFR）チロシンキナーゼを選択的に阻害し（EGFRチロシンキナーゼに対するIC50は0.027μmol/Lであり、ErbB2、KDR、Flt-1、Raf、MEK-1及びERK-2に対する阻害作用はその100分の1以下）、腫瘍細胞の増殖能を低下させる17)。また、DNA断片化18)及び組織形態学的観察19),20)に基づき、ゲフィチニブがアポトーシスを誘導するとの報告がある。さらに、血管内皮増殖因子（VEGF）の産生抑制を介して腫瘍内の血管新生を阻害することも報告されている21)。ゲフィチニブはこれらの作用に基づき悪性腫瘍の増殖抑制あるいは退縮を引き起こすものと考えられるが、腫瘍退縮の作用機序の詳細は不明である。

薬理作用

イレッサ錠250

in vitro系において、ゲフィチニブは口腔扁平上皮癌株KBのEGF刺激による増殖を阻害した（IC50：0.054μmol/L）17)。

ヒト腫瘍ヌードマウス移植系において、ゲフィチニブは12.5～200mg/kg/日の用量で非小細胞肺癌株A549、ヒト前立腺癌株Du145、ヒト外陰部腫瘍株A431、大腸癌株CR10、HCT15、HT29、LoVo、口腔扁平上皮癌株KB、卵巣癌株HX62に対して腫瘍増殖抑制作用を示した

動態

適応

小細胞癌でない肺癌　→　とくに腺癌に著効

化学療法が奏功しない患者

ゲフィニチブが奏効する患者

出典不明参考2

女性
低PS
非喫煙～軽度喫煙者
東洋人
腺癌

効能又は効果

イレッサ錠250

手術不能又は再発非小細胞肺癌

警告

イレッサ錠250

1. 本剤による治療を開始するにあたり、患者に本剤の有効性・安全性、息切れ等の副作用の初期症状、非小細胞肺癌の治療法、致命的となる症例があること等について十分に説明し、同意を得た上で投与すること。
2. 本剤の投与により急性肺障害、間質性肺炎があらわれることがあるので、胸部X線検査等を行うなど観察を十分に行い、異常が認められた場合には投与を中止し、適切な処置を行うこと。

また、急性肺障害や間質性肺炎が本剤の投与初期に発生し、致死的な転帰をたどる例が多いため、少なくとも投与開始後4週間は入院またはそれに準ずる管理の下で、間質性肺炎等の重篤な副作用発現に関する観察を十分に行うこと。

3. 特発性肺線維症、間質性肺炎、じん肺症、放射線肺炎、薬剤性肺炎の合併は、本剤投与中に発現した急性肺障害、間質性肺炎発症後の転帰において、死亡につながる重要な危険因子である。このため、本剤による治療を開始するにあたり、特発性肺線維症、間質性肺炎、じん肺症、放射線肺炎、薬剤性肺炎の合併の有無を確認し、これらの合併症を有する患者に使用する場合には特に注意すること。（「慎重投与」の項参照）
4. 急性肺障害、間質性肺炎による致死的な転帰をたどる例は全身状態の良悪にかかわらず報告されているが、特に全身状態の悪い患者ほど、その発現率及び死亡率が上昇する傾向がある。本剤の投与に際しては患者の状態を慎重に観察するなど、十分に注意すること。（「慎重投与」の項参照）
5. 本剤は、肺癌化学療法に十分な経験をもつ医師が使用するとともに、投与に際しては緊急時に十分に措置できる医療機関で行うこと。（「慎重投与」、「重要な基本的注意」及び「重大な副作用」の項参照）

注意

禁忌

副作用

重大な副作用

イレッサ錠250

1. 急性肺障害、間質性肺炎（1～10%未満）：急性肺障害、間質性肺炎があらわれることがあるので、胸部Ｘ線検査等を行うなど観察を十分に行い、異常が認められた場合には、投与を中止し、適切な処置を行うこと。
2. 重度の下痢（1%未満）：重度の下痢があらわれることがあるので、このような症状があらわれた場合には、速やかに適切な処置を行うこと。
3. 脱水（1%未満）：下痢、嘔気、嘔吐又は食欲不振に伴う脱水があらわれることがあるので、このような症状があらわれた場合には、速やかに適切な処置を行うこと。なお、脱水により腎不全に至った症例も報告されていることから、必要に応じて電解質や腎機能検査を行うこと。
4. 中毒性表皮壊死融解症（Toxic Epidermal Necrolysis：TEN）（1%未満）、皮膚粘膜眼症候群（Stevens-Johnson症候群）（1%未満）、多形紅斑（1%未満）：中毒性表皮壊死融解症、皮膚粘膜眼症候群、多形紅斑があらわれることがあるので、観察を十分に行い、異常が認められた場合には、投与を中止するなど適切な処置を行うこと。
5. 肝炎（1%未満）、肝機能障害（10%以上）、黄疸（1%未満）、肝不全（1%未満）：肝炎、AST（GOT）、ALT（GPT）、LDH、γ-GTP、Al-P、ビリルビンの上昇等を伴う肝機能障害、黄疸があらわれることがあり、肝不全に至った症例も報告されているので、本剤投与中は1～2ヵ月に1回、あるいは患者の状態に応じて肝機能検査を実施するなど観察を十分に行い、重度の肝機能検査値変動が認められた場合には、投与を中止するなど適切な処置を行うこと。（「重要な基本的注意」の項参照）
6. 血尿（1%未満）、出血性膀胱炎（1%未満）：血尿、出血性膀胱炎があらわれることがあるので、異常が認められた場合には、投与を中止するなど、適切な処置を行うこと。
7. 急性膵炎（1%未満）：急性膵炎があらわれることがあるので、観察を十分に行い、腹痛、血清アミラーゼ値の上昇等が認められた場合には投与を中止し、適切な処置を行うこと。
8. 消化管穿孔（1%未満）、消化管潰瘍（1%未満）、消化管出血（1%未満）：消化管穿孔、消化管潰瘍、消化管出血があらわれることがあるので、観察を十分に行い、異常が認められた場合には、内視鏡、腹部X線、CT等の必要な検査を行い、本剤の投与を中止するなど、適切な処置を行うこと。

相互作用

治療

250mg錠を1日一錠経口で服用

参考

イレッサ錠250

http://www.info.pmda.go.jp/go/pack/4291013F1027_1_25/4291013F1027_1_25?view=body

2. [charged] Small molecule epidermal growth factor receptor inhibitors for advanced non-small cell lung cancer - uptodate [1]

「nib」

　　[★]

受容体のリガンド結合部を標的とした小分子化合物。

nib

アキシチニブ axitinib
ボスチニブ bosutinib
ブリバニブ brivanib
カネルチニブ canertinib
セジラニブ cediranib
ダサチニブ dasatinib　チロシンキナーゼ阻害薬　イマチニブ抵抗性の慢性骨髄性白血病、再発又は難治性のフィラデルフィア染色体陽性急性リンパ性白血病
エルロチニブ erlotinib
ゲフィチニブ gefitinib
イマチニブ imatinib　チロシンキナーゼ阻害薬　CML、CKIT(CD117)陽性消化管間質腫瘍、
ラパチニブ lapatinib
レスタウルチニブ lestaurtinib
リニファニブ linifanib
ロナファーニブ lonafarnib
ネラチニブ neratinib
ニブリン nibrin
ニロチニブ nilotinib　チロシンキナーゼ阻害薬　イマチニブ抵抗性の慢性期又は移行期の慢性骨髄性白血病
パゾパニブ pazopanib
ペガプタニブ pegaptanib
ラニビズマブ ranibizumab
セマキシニブ semaxinib
ソラフェニブ sorafenib
スニチニブ sunitinib　VEGFRやPDGFRチロシンキナーゼ阻害薬　イマチニブ抵抗性の消化管間質腫瘍、根治切除不能又は転移性の腎細胞癌
ティピファニブ tipifarnib
バンデタニブ vandetanib
バタラニブ vatalanib

「上皮成長因子受容体阻害薬」

　　[★]

英: epidermal growth factor receptor inhibitor
関: 上皮成長因子受容体

薬理学

EGF受容体拮抗薬

BCR-ALB/C-KIT/PDGFR阻害薬

FLT3阻害薬

PKC412(midostaurin)

JAK2阻害薬
RAS/MAPキナーゼ経路阻害

mTOR阻害薬

rapamycin(sirolimus)
temsirolimus(CCI-779)
everolimus(RAD001)

[Pao2004-1] Pao W, Miller V, Zakowski M, et al. (September 2004). "EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib". Proceedings of the National Academy of Sciences of the United States of America 101 (36): 13306–11. doi:10.1073/pnas.0405220101. PMC 516528. PMID 15329413. Retrieved 2009-07-02.

[Sordella2004-2] Sordella R, Bell DW, Haber DA, Settleman J (August 2004). "Gefitinib-sensitizing EGFR mutations in lung cancer activate anti-apoptotic pathways". Science 305 (5687): 1163–7. doi:10.1126/science.1101637. PMID 15284455. |accessdate= requires |url= (help)

[3] Takimoto CH, Calvo E. "Principles of Oncologic Pharmacotherapy" in Pazdur R, Wagman LD, Camphausen KA, Hoskins WJ (Eds) Cancer Management: A Multidisciplinary Approach. 11 ed. 2008.

[Label2003-4] ttp://www.accessdata.fda.gov/drugsatfda_docs/label/2003/021399lbl.pdf

[5] ttp://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm110473.htm

[6] ttp://www.pharmac.govt.nz/2012/07/09/2012.07.10%20gefitinib%20funded.pdf

[7] ttp://www.bbc.co.uk/news/uk-scotland-edinburgh-east-fife-24021956

[8] Mok TS et al. Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma. N Eng J Med 2009; 361. 10.1056/NEJMoa0810699.

[AMH2004-9] Rossi S, editor. Australian Medicines Handbook 2004. Adelaide: Australian Medicines Handbook; 2004. ISBN 0-9578521-4-2.

Systematic (IUPAC) name


N-(3-chloro-4-fluoro-phenyl)-7-methoxy- 6-(3-morpholin-4-ylpropoxy)quinazolin-4-amine
Clinical data
Trade names	Iressa
AHFS/Drugs.com	monograph
MedlinePlus	a607002
Pregnancy cat.	C (Au), D (U.S.)
Legal status	S4 (Au), POM (UK), ℞-only (U.S.)
Routes	Oral
Pharmacokinetic data
Bioavailability	59% (oral)
Protein binding	90%
Metabolism	Hepatic (mainly CYP3A4)
Half-life	6–49 hours
Excretion	Faecal
Identifiers
CAS number	184475-35-2^Y
ATC code	L01XE02
PubChem	CID 123631
DrugBank	DB00317
ChemSpider	110217^Y
UNII	S65743JHBS^Y
KEGG	D01977^Y
ChEBI	CHEBI:49668^Y
ChEMBL	CHEMBL939^Y
Chemical data
Formula	C₂₂H₂₄ClFN₄O₃
Mol. mass	446.902 g/mol
SMILES COc1cc2c(cc1OCCCN3CCOCC3)c(ncn2)Nc4ccc(c(c4)Cl)F
InChI InChI=1S/C22H24ClFN4O3/c1-29-20-13-19-16(12-21(20)31-8-2-5-28-6-9-30-10-7-28)22(26-14-25-19)27-15-3-4-18(24)17(23)11-15/h3-4,11-14H,2,5-10H2,1H3,(H,25,26,27)^Y Key:XGALLCVXEZPNRQ-UHFFFAOYSA-N^Y
Y (what is this?) (verify)

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