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¾Æ½ÃµåºêÀÌÁÖ(¿¡ÅäÆ÷½Ãµå) ASIDE V INFU.VIAL.[Etoposide]
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µå·°ÀÎÆ÷¿¡¼´Â ÀǾàǰ ÀÎÅÍ³Ý ÆÇ¸Å¸¦ ÇÏÁö ¾Ê½À´Ï´Ù. |
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10 ¹ÙÀÌ¾Ë |
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8806449013708 |
8806449013722 |
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1 ¹ÙÀÌ¾Ë |
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8806449013708 |
8806449013715 |
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157101BIJ
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2. Åõ¿© ½Ã 100 mg´ç 250 mL ÀÌ»óÀÇ »ý¸®½Ä¿° ÁÖ»ç¾× µî ¼ö¾×¿¡ È¥ÇÕÇÏ¿© 30ºÐ ÀÌ»ó¿¡ °ÉÃÄ Á¡Àû Á¤¸ÆÁÖ»çÇÑ´Ù.
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3) ÀӺΠ¶Ç´Â ÀÓ½ÅÇϰí ÀÖÀ» °¡´É¼ºÀÌ ÀÖ´Â ¿©¼º |
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6) °í·ÉÀÚ
7) ¼Ò¾Æ(ÀÌ»ó¹ÝÀÀÀÇ ¹ßÇö¿¡ ƯÈ÷ ÁÖÀÇÇÑ´Ù.)
8) Àå±âÅõ¿© ȯÀÚ |
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(1) ¼ï(0.2%), ¾Æ³ªÇʶô½Ã¾ç Áõ»óÀ» ÀÏÀ¸Å³ ¼ö ÀÖÀ¸¹Ç·Î ÃæºÐÈ÷ °üÂûÇϰí, û»öÁõ, È£Èí°ï¶õ, ÈäºÎºÒÄè°¨, Ç÷¾ÐÀúÇÏ µîÀÇ Áõ»óÀÌ ³ªÅ¸³ª´Â °æ¿ì¿¡´Â Åõ¿©¸¦ ÁßÁöÇϰí ÀûÀýÇÑ Ã³Ä¡¸¦ ÇÑ´Ù.
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(1) ¶§¶§·Î BUN, Å©·¹¾ÆÆ¼´Ñ »ó½Â, ¿ä´Ü¹éÀÌ ³ªÅ¸³¯ ¼ö ÀÖ´Ù.
(2) ±Þ¼º½ÅºÎÀüÁõ : Á¶Ç÷¸ð¼¼Æ÷ À̽ÄÀ» À§ÇØ ¿¡ÅäÆ÷½Ãµå °í¿ë·®(2220 mg/m2) Åõ¿© ¹× Àü½ÅÁ¶»ç(total body irradiation) ÈÄ °¡¿ª¼º ±Þ¼º ½ÅºÎÀüÁõ ¹ßº´ÀÌ º¸°í µÇ¾ú´Ù. ±Þ¼º ½ÅºÎÀüÁõÀº µ¦½ºÆ®¶õ 40À» ÇÔÀ¯ÇÑ ¿¡ÅäÆ÷½Ãµå ¼ººÐÁ¦Á¦¸¦ °í¿ë·®À¸·Î Åõ¿©ÇÑ °Í°ú °ü·ÃµÇ¾î ÀÖ´Ù.
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7) ÇǺÎ
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8) Á¤½Å½Å°æ°è
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10) ÀüÇØÁú
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3. Àç¹ß¼º ¹× ÀüÀ̼º À§¾Ï, ÀüÀ̼º°áÀå¾Ï¿¡ º¹°³»·Î Åõ¿©ÇÑ Ç×¾ÏÁ¦¿¡ ´ëÇÏ¿©(2»ç·Ê)
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617 Àϵ¿ÆÄ¸ð·çºñ½ÅpfsÁÖ 50mg 1x1
421 ÀÌÇÇ¿¡½ºÁÖ 100mg 1x1
421 Áß¿Ü5-¿¡ÇÁÀ¯ÁÖ 250mg 1x1,500mg 1x1
421 Ǫ¶ó½Ã½ºÁÖ 10mg 1x1, 50mg 1x1
421 ÇǽùٴÒÁÖ 5ke : 1x1
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CT,Tumor marker
10/16 CA 19-9¡è
CT ÃÔ¿µ: No interval change of the intrahepatic biliary tree dilatation andhepatic cyst. Developed small amount of the ascites.... R/O Malignant naturedascites.
11/17 pain on shoulder area,mobility limitation
12/29 generalized valanceand weakness, pain shoulder
1/12 Care for intervalchecking
Mild abdominal distension is noted
PE : suspicious ascites, no liver palpable
CT ÃÔ¿µ: Abd.cavity³»¿¡ascites°¡ ¸¹ÀÌ Â÷ ÀÖÀ½.
¡æ Known patient of the stomach cancer
Hepatic splenic and peritoneal meta Rt. pleural effusion... Suggesting malignant natured.
1/14 Intraperitoneal chemoTx started, ascites +++
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started the interperitoneal chemo Tx
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2/19 discharged med
mildperitonitic symptoms sustained
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2Â÷(Çö Áø·áºÐ)
1/14
N/S 1L + placis 60mg
2/14
N/S 1L + placis 60mg
1/16
N/S 500ml + 5-FU 500mg
2/15
N/S 1L + 5-FU 750mg
1/17
N/S 1L + EPS 100mg
2/16
picibanil 5KE
1/18
N/S 1L + pharmorubicin 50mg
2/17
N/S 1L + pharmorubicin 50mg
1/19
picibanil 5KE
2/18
N/S 1L + EPS 100mg
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421 Áß¿Ü5-¿¡ÇÁÀ¯ÁÖ 250mg 1x4,500mg 1x4
421 Ǫ¶ó½Ã½ºÁÖ 10mg 1x1, 50mg 1x1
392 ³ªÀ̸°ÁÖ 15mg 2x1
[óġ ¹× ¼ö¼ú·á]
ÀÚ-706-³ª(±Þ¼ºº¹¸·Åõ¼®, Åõ¼®±³È¯) 1x4
ÀÚ-267-´Ù(°áÀåÀýÁ¦¼ú, ºÎºÐÀýÁ¦¼ú, ¸²ÇÁÀýû¼Ò¸¦ ÇÏ´Â °æ¿ì) 1x1
12/23 CC) bloody stool, Wt. loss
recently pain¡è, ascitis (+)
Dx)colon cancer or with liver metastasis
12/31 ÀÔ¿ø
CT ÃÔ¿µ : Suggesting ascending colon cancer with hepatic metastasis.
CA19-9 : 2427U/§¢(Âü°íÄ¡ : 0-39)
1/4 OP
Op name : palliative ileo-colectomy
(colon segmental resection)
post Op Dx
- ascending colon cancer with nearly complete obstruction, with multipleliver metastasis,
with peritoneal seeding (SB mesentery, omentum and paracolic gut), withrectal shelf(+)
1/5 Á¶Á÷º´¸® °Ë»ç (Colon, ascending, segmental resection)
¡æ Adenocarcinoma, moderate to poorlydifferentiated
Surgical margins, proximal and distal, resection : no tumor
Lymph node, pericolic dissection : adenocarcinoma,metastatic(3/7)
Mesenteric tissue, excision : adenocarcinoma, seeding
Appendix, appendectomy : no tumor
1/6 sl.dehydrated state withlarge amount of ascites
wound clear -> dressing change
1/9 gass pas(+) anddefecation with melena form
-> NPO continue till tonight
1/10 SOW and diet(LD) start
1/18 AST/ALT¡è, r-GTP¡è, WBC¡è, CEA:normal
CA19-9½ÉÇÔ. suggestive intra hepatic bile ductal cancerrather than metastasis cholangitis
1/24 decided to stent JPchemo Tx
Cisplatin through the JP tube injected
1/25 5-Fu IP chemo Tx
2/11 Chest PA : metastaticlesion both locus lung field, leg & foot edema
2/19 dyspnea½ÉÇÔ, edema½ÉÇÔ
urine output¡é, O2 inhalation¡è¡è
2/20 pain killer¡è, O2 inhalation¡è¡è
2/21 mental slightly dull,urine output¡é
2/22 13:14 expire
º¹°³»Ç×¾ÏÁ¦ Åõ¿©³»¿ª
1Â÷
1/24
N/S 1L + placis 60mg
1/25
H/D 1L + 5-FU 750mg
1/26
H/D 1L + 5-FU 750mg
1/27
H/D 1L + 5-FU 750mg, N/S 100mL + Nyrin 30mg
ÀÇ»ç¼Ò°ß¼
- »ó±âȯÀÚ´Â ¿ìÃø´ëÀå¿¡ Æó¼âÁ÷ÀüÀÇ °Å´ëÇÑ Á¾¾çÀÌ ÀÖ¾ú°í °£, Àå°£¸· ¹× º¹¸·, ¶ÇÇÑ °ñ¹Ý°³»¿¡µµ ÀüÀ̵ǾîÀÖÀ¸¸ç ¾Ï¼º º¹¼ö°¡ ÀÖ¾î ¿ÃÇØ 1¿ù 4ÀÏ ¿ìÃø ´ëÀåÀýÁ¦¼úÀ» ½ÃÇàÇÑ ÈÄ IP-CTx.¿Í º¹¼öõÀÚ¸¦ À§ÇÏ¿© J-P catheter¸¦ ¼³Ä¡ÇÏ¿´À½.
- IP-CTx.´Â ±âÁ¸ÈÇпä¹ýÀ¸·Î¼ ƯÈ÷ ¾Ç¼º º¹¼ö°¡ ÀÖ´Â °æ¿ì¿¡ systemicÀ¸·ÎÇÏ´Â º¸ÅëÀÇ Á¤¸Æ³» Á¡ÀûÄ¡·áº¸´Ù´Â local Áï º¹°À̳ª Èä°û³»·ÎÀÇ Á÷Á¢ÁÖÀÔ Ä¡·á°¡ ´õ È¿°úÀûÀÓ. ¶ÇÇÑ º¹¼öµµ 2-3ȸ Ä¡·á·Î ¹ß»ýÀÚü¸¦ ¾ïÁ¦ÇÏ´Â È¿°ú°¡ ÀÖÀ½. µû¶ó¼ ÀϹÝÁ¡ÀûÄ¡·á¸¦ ½ÃÇàÇÏ´Ù°¡µµ º¹¼ö°¡ ¹ß»ýÇϸé IP-CTx.·ÎÄ¡·áÇÏ´Â °ÍÀÌ ´õ È¿°úÀûÀÓ.
¡á Âü°í
¡Û ±¹¹Î°Ç°º¸Çè¿ä¾ç±Þ¿©ÀDZâÁØ¿¡°üÇѱÔÄ¢ [º°Ç¥1] ¿ä¾ç±Þ¿©ÀÇ Àû¿ë±âÁØ ¹× ¹æ¹ý 1,3
¡Û º¹°³»Ç׾Ͽä¹ý½Ã ¼ö±â·á ¹× Ä¡·áÀç·á »êÁ¤¹æ¹ý (º¸°Çº¹ÁöºÎ °í½Ã Á¦2004-36È£,'04.6.24)
¡Û cisplatin ÁÖ»çÁ¦ ¿ä¾ç±Þ¿©±âÁØ (º¸°Çº¹ÁöºÎ°í½Ã Á¦2001-28È£,'01.6.8)
¡Û 5-fluorouracil ÁÖ»çÁ¦ ¿ä¾ç±Þ¿©±âÁØ (º¸°Çº¹ÁöºÎ °í½Ã Á¦2001-28È£,'01.6.8)
¡Û etoposide ÁÖ»çÁ¦ ¿ä¾ç±Þ¿©±âÁØ (º¸°Çº¹ÁöºÎ°í½Ã Á¦2001-28È£,'01.6.8)
¡Û 5-FU + Ca. Leucovorin º´¿ë¿ä¹ý ¿ä¾ç±Þ¿©±âÁØ (º¸°Çº¹ÁöºÎ °í½Ã Á¦2001-28È£,'01.6.8)
¡Û ½Ä¾àûÀå Çã°¡»çÇ× (Ǫ¶ó½Ã½ºÁÖ, 5-¿¡ÇÁÀ¯ÁÖ, ÆÄ¸ð·çºñ½Å pfs ÁÖ,ÀÌÇÇ¿¡½º ÁÖ, ÇÇ½Ã¹Ù´Ò ÁÖ, ³ªÀ̸° ÁÖ).µî.
¡á ½ÉÀdz»¿ë
µ¿ »ç·ÊµéÀº Àç¹ß¼º ¹× ÀüÀ̼º À§¾Ï, ÀüÀ̼º °áÀå¾Ï¿¡ ÆÄ¸ð·çºñ½ÅÁÖ, ÀÌÇÇ¿¡½ºÁÖ, 5-¿¡ÇÁÀ¯ÁÖ, Ǫ¶ó½Ã½ºÁÖ, ÇǽùٴÒÁÖ, ³ªÀ̸°ÁÖ¸¦ 3Á¾¶Ç´Â 5Á¾ º´¿ëÇÏ¿© º¹°³» Åõ¿©ÇÑ °ÇÀ¸·Î, ¾Ï¼ºº¹¼ö°¡ ÀÖ¾îÅõ¿©ÇÏ¿´´Ù°í´Â Çϳª ÀÌ¹Ì °£ µî ŸºÎÀ§¿¡ ÀüÀ̵Ǿî systemic therapy°¡ ÇÊ¿äÇÑ »óÅ¿¡¼ ¿©·¯°¡Áö Ç×¾ÏÁ¦¸¦ º¹°³» º´¿ëÅõ¿©ÇÔÀº ½Ä¾àûÀå Çã°¡¹üÀ§µµ ¾Æ´Ï°í °ü·Ã±Ù°Åµµ ¹ÌÈíÇÏ¸ç °øÀÎµÈ Ä¡·á¹æ¹ýÀÌ ¾Æ´Ï¹Ç·Î ÀÎÁ¤ÇÏÁö ¾Æ´ÏÇÔ.
[2005.7.14 Áø·á½É»çÆò°¡À§¿øÈ¸]
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| DUR °ü·Ã °í½Ã |
[º´¿ë¿¬·É±Ý±â ÀǾàǰ / ÀӺαݱâ ÀǾàǰ / ºñ¿ëÈ¿°úÀû ÇÔ·® ÀǾàǰ / ¾ÈÀü¼º °ü·Ã ±Þ¿©ÁßÁö ÀǾàǰ]
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 | ÇмúÁ¤º¸ |
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| Ç׸ñ |
³»¿ë |
| DUR (ÀǾàǰ»ç¿ëÆò°¡) |
º´¿ë±Ý±â :
°í½ÃµÈ º´¿ë±Ý±â ³»¿ëÀº ¾ø½À´Ï´Ù.
[»óÈ£ÀÛ¿ë/º´¿ë±Ý±â°Ë»ö]
¿¬·É´ë±Ý±â :
°í½ÃµÈ ¿¬·É±Ý±â ³»¿ëÀº ¾ø½À´Ï´Ù.
[¿¬·É´ë±Ý±â»ó¼¼°Ë»ö]
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| Mechanism of Action |
Etoposide¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Etoposide inhibits DNA topoisomerase II, thereby inhibiting DNA synthesis at the premitotic stage of cell division. Etoposide is cell cycle dependent and phase specific, affecting mainly the S and G2 phases of cell division.
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| Pharmacology |
Etoposide¿¡ ´ëÇÑ Pharmacology Á¤º¸ Etoposide is an antineoplastic agent and an epipodophyllotoxin (a semisynthetic derivative of the podophyllotoxins). It inhibits DNA topoisomerase II, thereby inhibiting DNA synthesis. Etoposide is cell cycle dependent and phase specific, affecting mainly the S and G2 phases. Two different dose-dependent responses are seen. At high concentrations (10 µg/mL or more), lysis of cells entering mitosis is observed. At low concentrations (0.3 to 10 µg/mL), cells are inhibited from entering prophase. It does not interfere with microtubular assembly. The predominant macromolecular effect of etoposide appears to be the induction of DNA strand breaks by an interaction with DNA-topoisomerase II or the formation of free radicals.
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| Metabolism |
Etoposide¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 3A4 (CYP3A4)
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| Protein Binding |
Etoposide¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ 97%
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| Half-life |
Etoposide¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 4-12 hours
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| Absorption |
Etoposide¿¡ ´ëÇÑ Absorption Á¤º¸ Absorbed well, time to peak plasma concentration is 1-1.5 hrs. Mean bioavailability is 50%.
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| Pharmacokinetics |
EtoposideÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- Èí¼ö :
etoposide capsule : 50% (25-75 %) ; 200 mg ÀÌ»óÀÇ °í¿ë·®¿¡¼ ÇöÀúÈ÷ °¨¼Ò
etoposide phosphate : 68% (36-112 %)
À½½Ä¹° : ¿µÇâ¾øÀ½
- ºÐÆ÷ : IV :
³úô¼ö¾× : 10% ¹Ì¸¸
Vd : 7-17 L/m2
ºÐÆ÷ ¹Ý°¨±â : 1-1.5 ½Ã°£
- ´Ü¹é°áÇÕ : 97%
- ¹Ý°¨±â : 4-11 ½Ã°£ (¼Ò¾Æ : 3.37-5.8 ½Ã°£)
- ´ë»ç : °£´ë»ç
- ¼Ò½Ç : ½Å¹è¼³ (42-67 %), ´ãÁó¹è¼³ (6% ÀÌÇÏ), ´ëº¯¹è¼³ (0-16%)
ÃÑ Å¬¸®¾î·±½º : 16-36 mL/min/m2
Æò±Õ ½ÅŬ¸®¾î·±½º : 7-10 mL/min/m2
- ÃÖ°í Ç÷Áß³óµµ µµ´Þ : °æ±¸ : 1-1.5 ½Ã°£
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| Biotransformation |
Etoposide¿¡ ´ëÇÑ Biotransformation Á¤º¸ Primarily hepatic (through O-demethylation via the CYP450 3A4 isoenzyme pathway) with 40% excreted unchanged in the urine.
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| Toxicity |
Etoposide¿¡ ´ëÇÑ Toxicity Á¤º¸ Side effects include alopecia, constipation, diarrhea, nausea and vomiting and secondary malignancies (leukemia).
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| Drug Interactions |
Etoposide¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Aprepitant Aprepitant may change levels of chemotherapy agentCyclosporine Cyclosporine increases the effect of etoposideQuinupristin This combination presents an increased risk of toxicity
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CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸]
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| Food Interaction |
Etoposide¿¡ ´ëÇÑ Food Interaction Á¤º¸ Grapefruit and grapefruit juice should be avoided throughout treatment as grapefruit can decrease serum levels of this product.
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| Drug Target |
[Drug Target]
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| Description |
Etoposide¿¡ ´ëÇÑ Description Á¤º¸ A semisynthetic derivative of podophyllotoxin that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle. [PubChem]
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| Dosage Form |
÷°¡Á¦1 º¥Áú¾ËÄÚ¿Ã (ÁÖ»çÁ¦¿¡ ÇÑÇÔ.) ¡Û °æ°í
º¥Áú¾ËÄÚ¿ÃÀº ¹Ì¼÷¾Æ¿¡¼ Ä¡¸íÀûÀÎ °¡»Û È£ÈíÁõ»ó°ú ¿¬°üÀÌ ÀÖ´Â °ÍÀ¸·Î º¸°íµÇ¾ú´Ù.
¡Û ´ÙÀ½ ȯÀÚ¿¡´Â Åõ¿©ÇÏÁö ¸» °Í.
½Å»ý¾Æ, ¹Ì¼÷¾Æ(º¥Áú¾ËÄÚ¿ÃÀ» ÇÔÀ¯Çϰí ÀÖ´Ù.)
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| Drug Category |
Etoposide¿¡ ´ëÇÑ Drug_Category Á¤º¸ Antineoplastic Agents, PhytogenicNucleic Acid Synthesis Inhibitors
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| Smiles String Canonical |
Etoposide¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ COC1=CC(=CC(OC)=C1O)C1C2C(COC2=O)C(OC2OC3COC(C)OC3C(O)C2O)C2=CC3=C(OCO3)C=C12
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| Smiles String Isomeric |
Etoposide¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ COC1=CC(=CC(OC)=C1O)[C@H]1[C@@H]2[C@H](COC2=O)[C@H](O[C@@H]2O[C@@H]3CO[C@@H](C)O[C@H]3[C@H](O)[C@H]2O)C2=CC3=C(OCO3)C=C12
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| InChI Identifier |
Etoposide¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C29H32O13/c1-11-36-9-20-27(40-11)24(31)25(32)29(41-20)42-26-14-7-17-16(38-10-39-17)6-13(14)21(22-15(26)8-37-28(22)33)12-4-18(34-2)23(30)19(5-12)35-3/h4-7,11,15,20-22,24-27,29-32H,8-10H2,1-3H3/t11-,15+,20-,21-,22+,24-,25-,26-,27-,29+/m1/s1
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| Chemical IUPAC Name |
Etoposide¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 4'-demethyl-epipodophyllotoxin 9-[4,6-O-(R)-ethylidene-beta-D-glucopyranoside], 4'-(dihydrogen phosphate)
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| Drug-Induced Toxicity Related Proteins |
ETOPOSIDE ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:p44-extracellular signal receptor-activated kinase 2 Drug:etoposide Toxicity:apoptotic cell death and DNA damage. [¹Ù·Î°¡±â] Replated Protein:Mitogen-activated protein kinase p42 Drug:etoposide Toxicity:apoptotic cell death and DNA damage. [¹Ù·Î°¡±â] Replated Protein:SAPK enzymes p46 Drug:etoposide Toxicity:apoptotic cell death and DNA damage. [¹Ù·Î°¡±â] Replated Protein:DNA topoisomerase 2-alpha Drug:etoposide Toxicity:DNA damage and cell death. [¹Ù·Î°¡±â] Replated Protein:DNA topoisomerase 2 Drug:etoposide Toxicity:apoptosis. [¹Ù·Î°¡±â] ETOPOSIDE (VP16) ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Caspase-8 Drug:etoposide (VP16) Toxicity:cell death. [¹Ù·Î°¡±â] Replated Protein:B-cell receptor-associated protein 31(BAP31) Drug:etoposide (VP16) Toxicity:cell death. [¹Ù·Î°¡±â] Replated Protein:Caspase-8 Drug:etoposide (VP16) Toxicity:cell death. [¹Ù·Î°¡±â] Replated Protein:Caspase-3 Drug:etoposide (VP16) Toxicity:cell death. [¹Ù·Î°¡±â] ETOPOSIDE (VP-16) ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Apoptosis regulator Bcl-2 Drug:etoposide (VP-16) Toxicity:cytotoxicity. [¹Ù·Î°¡±â] Replated Protein:Hypoxanthine-guanine phosphoribosyltransferase Drug:etoposide (VP-16) Toxicity:etoposide (VP-16)-induced DNA recombination . [¹Ù·Î°¡±â] Replated Protein:Apoptosis regulator Bcl-2 Drug:etoposide (VP-16) Toxicity:VP-16-induced genetic recombination, mutation, and cytotoxicity. [¹Ù·Î°¡±â]
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| ½Å¾à¼Ò°³ |
Etoposide (ÀÌÇÇ¿¡½ºÁÖ)
±¸¼º
- ¿¯Àº Ȳ»öÀÇ Á¡¼ºÀÌ ÀÖ´Â etoposide°¡ 1vial¿¡100mg/5ml µé¾îÀÖ´Ù.
ÀûÀÀÁõ
- Æó¼Ò¼¼Æ÷¾Ï, ¾Ç¼ºÀÓÆÄÁ¾, ±Þ¼º¹éÇ÷º´, °íȯÁ¾¾ç, ¹æ±¤¾Ï, À¶¸ð¼º Áúȯ
ÀÛ¿ë±âÀü
- Etoposide´Â Podophyllum platum°úPodophyllum emodiÀǽŰ»Ñ¸®·ÎºÎÅÍÀ¯µµÇѹÝÇÕ¼ºÈÇÕ¹°·Î½á¼¼Æ÷ÁÖ±âÁß S±âÈĹݰú G2±â¿¡ ÀÛ¿ëÇÏ¿© DNA »ç½½ÀÇ Àý´ÜÀ» À¯µµÇÔÀ¸·Î½á¼¼Æ÷µ¶¼ºÀ» ¹ßÈÖÇÑ´Ù.
¿ë¹ý/¿ë·®
- 60-100mg/§³À» 5Àϰ£ ¿¬¼Ó Á¡Àû Åõ¿©Çϰí 3ÁÖ°£ ÈÞ¾à.
¿ë·®Á¶Àý
- ½ÅÀå¾Ö: Clcr15-50§¢/min ÀÏ ¶§ 75%·Î ¿ë·® °¨·®.
ÁÖ»ç¾× Á¶Á¦
- °áÁ¤ÀÌ ¼®ÃâµÉ ¼ö ÀÖÀ¸¹Ç·Î 0.2mg/ml~0.4mg/mlÀÇ ³óµµ·Î Èñ¼®ÇØ¾ß ÇÑ´Ù.
°æ°í
- ÀúÇ÷¾ÐÀÇ °¡´É¼ºÀ» ÁÙÀ̱â À§ÇØ 30~60ºÐ¿¡ °ÉÃļ õõÈ÷ Åõ¿©ÇÑ´Ù.
- Phosphatase¸¦ ¾ïÁ¦ÇÏ´Â ¾à¹°, °í³óµµÀÇ cyclosporin A¿ÍÀÇ º´¿ëÀ» ÇÇÇÑ´Ù.
ÈçÇÑ ºÎÀÛ¿ë
- ÇǺΰè: Å»¸ð
- ³»ºÐºñ°è: ¶³¸²
- ¼Òȱâ°è: ¼³»ç, Á¡¸· ¿°Áõ, ½Ä¿å°¨Åð, ¿À½É, ±¸Åä
- ½Å°æ°è: ¹«±â·ÂÁõ
- ±âŸ: ¿, ±Çۨ
½É°¢ÇÑ ºÎÀÛ¿ë
- ½ÉÇ÷°ü°è: ¿ïÇ÷¼º ½ÉºÎÀü, ½É±Ù°æ»ö
- ÇǺΰè: Stevens-Johnson ÁõÈıº, toxic epidermalnecrolysis
- ±Þ¼º ¹éÇ÷º´(rare), °ñ¼ö¾ïÁ¦, °£µ¶¼º, ¸é¿ª°ú¹Î¹ÝÀÀ
Pregnancy Category
- FDA category: D
º¸°ü
- ½Ç¿Âº¸°ü(25¡É ÀÌÇÏ)
Reference
- ÀÌÇÇ¿¡½ºÁÖ insert paper
- Micromedex
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µå·°ÀÎÆ÷ ÀǾàÇмúÁ¤º¸´Â ½ÄǰÀǾàǰ¾ÈÀüóÀÇ Á¦Ç°Çã°¡»çÇ×, Çмú¹®Çå, Á¦¾àȸ»ç Á¦°øÁ¤º¸ µîÀ» ±Ù°Å·Î ÀÛ¼ºµÈ Âü°í Á¤º¸ÀÔ´Ï´Ù.
Á¤º¸ÀÇ Á¤È®¼ºÀ» À§ÇØ ³ë·ÂÇϰí ÀÖÀ¸³ª ÆíÁý»óÀÇ ¿À·ù, Çã°¡»çÇ× º¯°æ, Ãß°¡ÀûÀÎ Çмú¿¬±¸ ¶Ç´Â Àӻ󿬱¸ ¹ßÇ¥ µîÀ¸·Î ÀÎÇØ ¹ß»ýÇÏ´Â ¹®Á¦¿¡ ´ëÇØ µå·°ÀÎÆ÷´Â
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ÀüÈ: 02-3486-1061 ¤Ó À̸ÞÀÏ: webmaster@druginfo.co.kr
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The database contains the following fields: The generic name of each chemical For module A10 (liver enzyme composite module): Overall activity category for each compound (A for active, M for marginally active, or I for inactive) based on the number of active and marginally active scores for each compound at the five individual endpoints (see research article for full description of method) Number of endpoints at which each compound is marginally active (M) Number of endpoints at which each compound is active (A) For modules A11 to A15 (alkaline phosphatase increased, SGOT increased, SGPT increased, LDH increased, and GGT increased, respectively): Overall activity category for each compound (A for active, M for marginally active, or I for inactive) based on the RI and ADR values (see the research article for full description of method) Number of ADR reports for each compound, given as <4 or ¡Ã4 Reporting Index value for each compound, except where no shipping units were available (NSU) Group 1 comprises of compounds for which ADR data were available for the first five years of marketing, so when no ADR reports were listed during this period the compounds were evaluated as inactive. Group 2 comprises of compounds for which a 'steady state' period of ADR data were available (1992-1996). In cases where no ADR reports were filed during this period, the compounds were scored as 'NA' (data not available) since they may have had one or more ADR reports during their first five years of marketing which should not be negated by a lack of ADR reports during the steady-state period. ETOPOSIDE[GGT Increase][Composite Activity](Score) I(Marginal) 0(Active) 0[Alkaline Phosphatase Increase](Activity Score) I(Number of Rpts) <4(Index value) 0.8[SGOT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0.4[SGPT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0[LDH Increase](Activity Score) I(Number of Rpts) <4(Index value) 0.4[GGT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0
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