|
|
|
|
|
À¯·áȸ¿ø °áÀç½Ã¿¡´Â º¸´Ù ´Ù¾çÇÑ ¾à¹°Á¤º¸¸¦
ÀÌ¿ëÇÏ½Ç ¼ö ÀÖ½À´Ï´Ù.
À¯·áÁ¤º¸¸ñ·ÏÀº Àü¹®È¸¿øÀ¸·Î
·Î±×ÀÎ ÇϽøé È®ÀÎ °¡´ÉÇÕ´Ï´Ù.
|
|
|
 | Çã°¡Á¤º¸ |
|
|
| Ç׸ñ |
³»¿ë |
û±¸ÄÚµå(KDÄÚµå) ºñ±Þ¿©Á¡°ËÄÚµå »óÇÑ±Ý¾× |
641803650
[º¸ÇèÄڵ忡 µû¸¥ ¾àǰ±âº»Á¤º¸ Á÷Á¢Á¶È¸]
[ºñ±Þ¿©]
[»óº´ÄÚµåÁ¶È¸]
[Áúº´ÄÚµåÁ¶È¸]
|
| ºü¸¥Á¶È¸ |
|
| Á¦Ç°¼º»ó |
¹é»ö-¹Ì¹é»öÀÇ ¿¬°íÁ¦ [Á¦ÇüÁ¤º¸ È®ÀÎ] |
| Æ÷À塤À¯Åë´ÜÀ§ |
ÀÚ»çÆ÷Àå´ÜÀ§¿¡ µû¸§ |
| Æ÷À塤ÄÚµå´ÜÀ§ |
| ¾àǰ±Ô°Ý |
´ÜÀ§ |
Æ÷ÀåÇüÅ |
´ëÇ¥ÄÚµå |
Ç¥ÁØÄÚµå |
ºñ°í |
| 10±×·¥ |
1 °³ |
Æ©ºê |
8806418036509 |
8806418036516 |
|
|
| ÁÖ¼ººÐÄÚµå |
346500COM
[µ¿ÀÏÇÑ ÁÖ¼ººÐÄڵ带 °¡Áø ¿À¸®Áö³¯ ¶Ç´Â Á¦³×¸¯ ÀǾàǰ Á¶È¸]
|
| Çã°¡»çÇ× ¿ø¹®Á¶È¸ |
[Çã°¡»çÇ× ¿ø¹®Á¶È¸]
|
| È¿´ÉÈ¿°ú |
[ÀûÀÀÁõ º° °Ë»ö]
³×¿À¸¶À̽а¨¼ö¼º ¼¼±Õ¿¡ ÀÇÇØ 2Â÷ °¨¿°µÈ ÄÚ¸£Æ¼ÄÚÀÌµå ¹ÝÀÀ¼º ÇǺÎÁúȯÀÇ Ãʱâ Ä¡·á : ÇǺο°, °¨¿°µÈ »óó
|
| ¿ë¹ý¿ë·® |
* Àý´ë ÀÓÀǺ¹¿ëÇÏÁö ¸¶½Ã°í ¹Ýµå½Ã ÀÇ»ç ¶Ç´Â ¾à»ç¿Í »ó´ãÇϽñ⠹ٶø´Ï´Ù.
[󹿾à¾î]
1ÀÏ 1¢¦2ȸ Àû´ç·®À» ȯºÎ¿¡ ¹Ù¸¥´Ù.
|
| ±Ý±â |
1) ¼¼±Õ(ÇǺΰáÇÙ, ¸Åµ¶)¤ýÁø±Õ(ĵð´ÙÁõ, ¹é¼± µî)¤ý¹ÙÀÌ·¯½º(´ë»óÆ÷Áø, ´Ü¼øÆ÷Áø, ¼öµÎ, Á¾ µÎÁõ µî)¤ýµ¿¹°(¿È, »ç¸é¹ßÀÌ µî)¼º ÇǺΰ¨¿°Áõ ȯÀÚ(Áõ»óÀÌ ¾Ç鵃 ¼ö ÀÖ´Ù)
2) ÀÌ ¾à ¶Ç´Â ÀÌ ¾à ¼ººÐ¿¡ °ú¹ÎÁõ ¹× ±× º´·ÂÀÌ Àִ ȯÀÚ
3) °í¸·Ãµ°øÀÌ ÀÖ´Â ½ÀÁø¼º ¿ÜÀ̵µ¿° ȯÀÚ(õ°øºÎÀ§ÀÇ Ä¡À¯Áö¿¬ÀÌ ³ªÅ¸³¯ ¼ö ÀÖ´Ù)
4) ±Ë¾ç(º£Ã¼Æ®º´ Á¦¿Ü), Á¦2µµ ½ÉÀ缺 ÀÌ»óÀÇ È»ó¤ýµ¿»óȯÀÚ(ÇǺÎÀç»ýÀÌ ¾ïÁ¦µÇ¾î Ä¡À¯ °¡ Áö¿¬µÉ ¼ö ÀÖ´Ù)
5) ÀÔÁÖÀ§ÇǺο°, º¸Åë¿©µå¸§, ÁÖ»ç(rosacea) ȯÀÚ
6) ½ºÆ®·¾Å丶À̽Å, Ä«³ª¸¶À̽Å, °ÕŸ¸¶À̽Å, ³×¿À¸¶À̽Šµî ¾Æ¹Ì³ë±Û·çÄÚ»çÀ̵å°è Ç×»ý ¹°Áú ¶Ç´Â ¹Ù½ÃÆ®¶ó½Å¿¡ ÀÇÇÑ °ú¹ÎÁõÀÇ ±â¿Õ·ÂÀÚ
7) ´« ¶Ç´Â ´«ÁÖÀ§
8) À¯¹æ ºÎÀ§¿¡ »óó°¡ Àִ ȯÀÚ(¼öÀ¯½Ã À¯¾Æ¿¡°Ô À¯À﵃ À§ÇèÀÌ ÀÖ´Ù)
|
| ½ÅÁßÅõ¿© |
1) ÀӺΠ¶Ç´Â ÀÓ½ÅÇϰí ÀÖÀ» °¡´É¼ºÀÌ ÀÖ´Â ºÎÀÎ ¹× ¼öÀ¯ºÎ
2) À¯¤ý¼Ò¾Æ
3) ÀÌ ¾àÀº ÇÁ·ÎÇÊ·»±Û¸®ÄÝÀ» ÇÔÀ¯Çϰí ÀÖÀ¸¹Ç·Î ÀÌ ¼ººÐ¿¡ °ú¹ÎÇϰųª ¾Ë·¹¸£±â º´·Â ÀÌ Àִ ȯÀÚ¿¡´Â ½ÅÁßÈ÷ Åõ¿©ÇÑ´Ù.
|
| ÀÌ»ó¹ÝÀÀ |
1) ÇǺÎ
¨ç °¨¿°Áõ : ÇǺÎÀÇ ¼¼±Õ¼º(Àü¿°¼º³ó°¡Áø, ¸ð³¶¿° µî), ¹ÙÀÌ·¯½º¼º °¨¿°ÁõÀÌ ³ªÅ¸³¯ ¼ö ÀÖ´Ù[¹ÐºÀºØ´ë¹ý(ODT)ÀÇ °æ¿ì ³ªÅ¸³ª±â ½±´Ù]. ÀÌ¿Í °°Àº Áõ»óÀÌ ³ªÅ¸³¯ °æ¿ì¿¡´Â ÀûÀýÇÑ Ç×±ÕÁ¦³ª Ç×Áø±ÕÁ¦µîÀ» º´¿ëÇϰí Áõ»óÀÌ ½Å¼ÓÈ÷ °³¼±µÇÁö ¾ÊÀ» °æ¿ì¿¡´Â »ç ¿ëÀ» ÁßÁöÇÑ´Ù.
¨è ÀϹÝÀû ÇǺÎÁõ»ó : ¸ð³¶¿°, ºÎ½º·³, ÇǺÎÀÚ±Ø, ÀÚÅë, ¹ß¿, ÀÛ¿°¨, ¹ßÁø¤ý¹ßÀû, È«Á¶, °¡·Á¿ò, ÇǺΰÇÁ¶, ³óÆ÷¼ºÇǺο°, ¾Ë·¹¸£±â¼º Á¢ÃËÇǺο°, 2Â÷°¨¿°, ÇǺΰÅÄ¥¾îÁü, ¶¡ ¶ì, »óó¾ÇÈ, ¿åâ, ³óÆ÷Áõ µîÀÇ Áõ»óÀÌ ³ªÅ¸³ª´Â °æ¿ì¿¡´Â »ç¿ëÀ» ÁßÁöÇϰí ÀÇ»ç ¶Ç´Â ¾à»ç¿Í »ó´ãÇÑ´Ù.
¨é Àå±â¿¬¿ë : ½ºÅ×·ÎÀ̵强 ¿©µå¸§, ½ºÅ×·ÎÀ̵强 ÇǺÎ(ÇǺÎÀ§Ãà, ¸ð¼¼Ç÷°üÈ®Àå, ÀÚ¹Ý), ½ºÅ×·ÎÀ̵强 ÁÖ»ç, ÀÔÁÖÀ§ÇǺο°(ÀÔÁÖÀ§¤ý¾È¸éÀüü¿¡ È«¹Ý, ±¸Áø, ¸ð¼¼Ç÷°üÈ®Àå, µüÁö, Àμ³), ¾î¸°¼±(åÛ×÷àÈ)¾ç ÇǺκ¯È, ´Ù¸ð, »ö¼ÒÅ»½Ç µîÀÌ ³ªÅ¸³¯ ¼ö ÀÖ´Ù. ÀÌ·¯ÇÑ Áõ »óÀÌ ³ªÅ¸³¯ °æ¿ì¿¡´Â õõÈ÷ »ç¿ë·®À» ÁÙ¿© ÄÚ¸£Æ¼ÄÚÀ̵带 ÇÔÀ¯ÇÏÁö ¾ÊÀº ¾àÀ¸·Î ¹Ù²Ù¾î »ç¿ëÇÑ´Ù.
2) ³»ºÐºñ°è : ´ë·® ¶Ç´Â Àå±â°£¿¡ °ÉÄ£ ±¤¹üÀ§ÇÑ »ç¿ë, ¹ÐºÀºØ´ë¹ý¿¡ ÀÇÇØ ÄÚ¸£Æ¼ÄÚÀÌ µå Àü½ÅÅõ¿©¿Í °°Àº ³úÇϼöü¤ýºÎ½ÅÇÇÁú°è ±â´ÉÀÇ ¾ïÁ¦¸¦ °¡Á®¿Ã ¼ö ÀÖÀ¸¹Ç·Î ÁÖÀÇÇÑ ´Ù.
3) ´« : ¾È°Ë ÇǺο¡ »ç¿ë½Ã ¾È¾Ð »ó½Â, ³ì³»ÀåÀ» ÀÏÀ¸Å³ ¼ö ÀÖÀ¸¹Ç·Î ÁÖÀÇÇÑ´Ù. ´ë·® ¶Ç´Â Àå±â°£¿¡ °ÉÄ£ ±¤¹üÀ§ÇÑ »ç¿ë, ƯÈ÷ ¹ÐºÀºØ´ë¹ýÀ» »ç¿ëÇÒ °æ¿ì Èij¶ÇϹ鳻Àå, ³ì³»Àå µîÀÌ ³ªÅ¸³¯ ¼ö ÀÖ´Ù. ºóµµºÒ¸íÀÇ ½Ã¾ßÈ帲ÀÌ ³ªÅ¸³¯ ¼ö ÀÖ´Ù.
4) ±Õ±³´ëÇö»ó : µå¹°°Ô ÀÌ ¾à¿¡ ´ëÇÏ¿© ºñ°¨¼ö¼º±Õ¿¡ ÀÇÇÑ °¨¿°ÁõÀ» ÀÏÀ¸Å³ ¼ö ÀÖÀ¸¹Ç ·Î ÀÌ·¯ÇÑ °æ¿ì¿¡´Â »ç¿ëÀ» ÁßÁöÇÑ´Ù.
5) ½ÅÀå¾Ö, ³Ã» µîÀÌ ³ªÅ¸³¯ ¼ö ÀÖÀ¸¹Ç·Î Àå±â¿¬¿ëÀ» ÇÇÇÑ´Ù.
4. ÀϹÝÀû ÁÖÀÇ
|
|
|
 | Á¤º¸¿ä¾à |
|
|
|
µå·°ÀÎÆ÷ ÀǾàǰ ¿ä¾à/»ó¼¼Á¤º¸
|
|
 | ÄÚµå ¹× ºÐ·ùÁ¤º¸ |
|
|
| |
|
 | Á¦Ç°Á¤º¸ |
|
|
|
|
 | º¹¾àÁ¤º¸ |
|
|
| Ç׸ñ |
³»¿ë |
| LACTmed ¹Ù·Î°¡±â |
[¹Ù·Î°¡±â]
|
| ¾à¸®ÀÛ¿ë |
À¯·áÁ¤º¸ÀÔ´Ï´Ù.
|
| Ãà¾àº¹¾àÁöµµ |
À¯·áÁ¤º¸ÀÔ´Ï´Ù.
|
| º¹¾àÁöµµ |
À¯·áÁ¤º¸ÀÔ´Ï´Ù.
|
| ÀӺο¡´ëÇÑÅõ¿© |
| * |
ÀüüÀӽŠ±â°£º°·Î ¿©·¯µî±ÞÀÌ Á¸ÀçÇÒ ¼ö ÀÖÀ¸¸ç °¡Àå À§Çèµµ°¡ ³ôÀº Á¤º¸¸¸ º¸¿©Áý´Ï´Ù. ´Ü, º¹ÇÕÁ¦ÀÇ °æ¿ì ¸ðµç º¹ÇÕÁ¦¼ººÐ¿¡ ´ëÇÑ ÀÓºÎÅõ¿©µî±ÞÀÌ Ç¥½ÃµÈ°ÍÀº Àý´ë ¾Æ´Ï¸ç Ç¥½ÃµÈ°ÍÁß¿¡ °¡Àå À§Çèµµ°¡ ³ôÀº Á¤º¸¸¸ ³ªÅ¸³³´Ï´Ù.
|
|
|   |
 FDA : Cµî±Þ
(topical )
|
|
| * |
»ó±â ÀÓºÎÅõ¿©¿¡ ´ëÇÑ Á¤º¸´Â Àü»êó¸® µÇ¸é¼ ÀÔ·Â ¿À·ù °¡´É¼ºÀÌ Á¸ÀçÇÕ´Ï´Ù. ¿À·ù °¡´É¼ºÀ» ÃÖ¼ÒÈÇϱâ À§ÇÏ¿© ¸¹Àº ³ë·ÂÀ» ±â¿ïÀ̰í ÀÖÀ¸³ª, ±× Á¤È®¼º¿¡ ´ëÇÏ¿© È®½ÅÀ» µå¸± ¼ö ¾ø½À´Ï´Ù. ÀÌ¿¡ ´ëÇØ ȸ»ç´Â Ã¥ÀÓÀ» ÁöÁö ¾Ê½À´Ï´Ù.
|
| * |
¹Ýµå½Ã °ø½Å·Â ÀÖ´Â ¹®ÇåÀ» ´Ù½Ã Çѹø Âü°í ÇϽñ⠹ٶó¸ç ÀÇ»ç ¶Ç´Â ¾à»çÀÇ ÆÇ´Ü¿¡ µû¶ó Åõ¿©¿©ºÎ°¡ °áÁ¤µÇ¾î¾ß ÇÕ´Ï´Ù.
|
|
|
| Pharmacokinetics |
À¯·áÁ¤º¸ÀÔ´Ï´Ù.
|
| Á¦Çüº° º¹¾àÁöµµ |
[¿¬°í] |
| º¸°ü»ó ÁÖÀÇ |
|
| Á¶Á¦½Ã ÁÖÀÇ |
|
|
|
 | ½É»çÁ¤º¸ |
|
|
|
|
 | ÇмúÁ¤º¸ |
|
|
| 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]
|
| Mechanism of Action |
Hydrocortisone¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In another words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.
Neomycin¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Aminoglycosides like neomycin "irreversibly" bind to specific 30S-subunit proteins and 16S rRNA. Specifically neomycin binds to four nucleotides of 16S rRNA and a single amino acid of protein S12. This interferes with decoding site in the vicinity of nucleotide 1400 in 16S rRNA of 30S subunit. This region interacts with the wobble base in the anticodon of tRNA. This leads to interference with the initiation complex, misreading of mRNA so incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides and the breakup of polysomes into nonfunctional monosomes.
|
| Pharmacology |
Hydrocortisone¿¡ ´ëÇÑ Pharmacology Á¤º¸ Hydrocortisone is the most important human glucocorticoid. It is essential for life and regulates or supports a variety of important cardiovascular, metabolic, immunologic and homeostatic functions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger a variety of important cardiovascular, metabolic, immunologic and homeostatic effects. Glucocorticoids are distinguished from mineralocorticoids and sex steroids by having different receptors, target cells, and effects. Technically, the term corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid. Glucocorticoids suppress cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most important of which is the IL-2. Reduced cytokine production limits T cell proliferation. Glucocorticoids also suppress humoral immunity, causing B cells to express lower amounts of IL-2 and IL-2 receptors. This diminishes both B cell clonal expansion and antibody synthesis. The diminished amounts of IL-2 also leads to fewer T lymphocyte cells being activated.
Neomycin¿¡ ´ëÇÑ Pharmacology Á¤º¸ Neomycin is an aminoglycoside antibiotic. Aminoglycosides work by binding to the bacterial 30S ribosomal subunit, causing misreading of t-RNA, leaving the bacterium unable to synthesize proteins vital to its growth. Aminoglycosides are useful primarily in infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. In addition, some mycobacteria, including the bacteria that cause tuberculosis, are susceptible to aminoglycosides. Infections caused by Gram-positive bacteria can also be treated with aminoglycosides, but other types of antibiotics are more potent and less damaging to the host. In the past the aminoglycosides have been used in conjunction with penicillin-related antibiotics in streptococcal infections for their synergistic effects, particularly in endocarditis. Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi and viruses.
|
| Metabolism |
Hydrocortisone¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 3A4 (CYP3A4)
Neomycin¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Not Available
|
| Protein Binding |
Hydrocortisone¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ 95%
Neomycin¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ Protein binding studies have shown that the degree of aminoglycoside protein binding is low and, depending upon the methods used for testing, may be between 0% and 30%.
|
| Half-life |
Hydrocortisone¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 6-8 hours
Neomycin¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 2 to 3 hours
|
| Absorption |
Hydrocortisone¿¡ ´ëÇÑ Absorption Á¤º¸ Topical corticosteroids can be absorbed from normal intact skin. Inflammation and/or other disease processes in the skin increase percutaneous absorption.
Neomycin¿¡ ´ëÇÑ Absorption Á¤º¸ Poorly absorbed from the normal gastrointestinal tract. Although only approximately 3% of neomycin is absorbed through intact intestinal mucosa, significant amounts may be absorbed through ulcerated or denuded mucosa or if inflammation is present.
|
| Pharmacokinetics |
Neomycin SulfateÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- Èí¼ö : °æ±¸, °æÇÇ : Èí¼öµÇ´Â ¾çÀÌ ¹Ì¹ÌÇÏ´Ù. (3%)
- ºÐÆ÷ : ºÐÆ÷¿ëÀû : 0.36 L/kg
- ´ë»ç : ¼Ò·®ÀÌ °£¿¡¼ ´ë»çµÈ´Ù.
- ¹Ý°¨±â : 3 ½Ã°£ (³ªÀÌ¿Í ½Å±â´É¿¡ ÀÇÁ¸)
- Ç÷ÁßÃÖ°í³óµµ µµ´Þ½Ã°£ :
- °æ±¸ : 1-4 ½Ã°£
- ±ÙÀ°ÁÖ»ç : 2 ½Ã°£ À̳»
- ¼Ò½Ç :
- ÁÖ»çÁ¦ : ½Å¹è¼³ (30-50%°¡ ¹Ìº¯Èü·Î ¹è¼³)
- °æ±¸ : 97%°¡ ¹Ìº¯Èü·Î º¯¹è¼³
Hydrocortisone acetateÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- Èí¼ö : Á÷ÀåÀ» Á¦¿ÜÇÑ ¸ðµç Åõ¿©°æ·Î¿¡¼ ºü¸£°Ô Èí¼öµÈ´Ù.
- ´ë»ç : °£¿¡¼ ´ë»çµÈ´Ù.
- »ý¸®Àû ¹Ý°¨±â : 8¡12½Ã°£
- ¼Ò½Ç : ÁÖ·Î 17-hydroxysteroids¿Í 17-ketosteroidsÀÇ ÇüÅ·Π½Å¹è¼³µÈ´Ù.
- ¿ëÇØ¼ºÀÌ Å« ´Ù¸¥ ¾à¹°°ú ºñ±³ÇßÀ» ¶§ hydrocortisone acetate´Â ÀÛ¿ë¹ßÇö½Ã°£Àº ´À¸®Áö¸¸ ÀÛ¿ëÁö¼Ó½Ã°£ÀÌ ±æ´Ù.
- Hydrocortisone sodium succinate´Â ¹°¿¡ ½±°Ô ³ì¾Æ »¡¸® Ȱ¼ºÈµÈ´Ù.
|
| Biotransformation |
Hydrocortisone¿¡ ´ëÇÑ Biotransformation Á¤º¸ Primarily hepatic via CYP3A4
Neomycin¿¡ ´ëÇÑ Biotransformation Á¤º¸ Neomycin undergoes negligible biotransformation after parenteral administration.
|
| Toxicity |
Hydrocortisone¿¡ ´ëÇÑ Toxicity Á¤º¸ Side effects include inhibition of bone formation, suppression of calcium absorption and delayed wound healing
Neomycin¿¡ ´ëÇÑ Toxicity Á¤º¸ LD50 = 200 mg/kg (rat). Because of low absorption, it is unlikely that acute overdosage would occur with oral neomycin. However, prolonged administration could result in sufficient systemic drug levels to produce neurotoxicity, ototoxicity and/or nephrotoxicity.
|
| Drug Interactions |
Hydrocortisone¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Ambenonium The corticosteroid decreases the effect of anticholinesterasesEdrophonium The corticosteroid decreases the effect of anticholinesterasesNeostigmine The corticosteroid decreases the effect of anticholinesterasesPyridostigmine The corticosteroid decreases the effect of anticholinesterasesAspirin The corticosteroid decreases the effect of salicylatesBismuth Subsalicylate The corticosteroid decreases the effect of salicylatesSalicylate-magnesium The corticosteroid decreases the effect of salicylatesSalicylate-sodium The corticosteroid decreases the effect of salicylatesSalsalate The corticosteroid decreases the effect of salicylatesTrisalicylate-choline The corticosteroid decreases the effect of salicylatesWarfarin The corticosteroid alters the anticoagulant effectAcenocoumarol The corticosteroid alters the anticoagulant effectDicumarol The corticosteroid alters the anticoagulant effectAnisindione The corticosteroid alters the anticoagulant effectCholestyramine Cholestyramine decreases the effect of hydrocortisoneColestipol Cholestyramine decreases the effect of hydrocortisoneAmobarbital The barbiturate decreases the effect of the corticosteroidAprobarbital The barbiturate decreases the effect of the corticosteroidButabarbital The barbiturate decreases the effect of the corticosteroidButalbital The barbiturate decreases the effect of the corticosteroidButethal The barbiturate decreases the effect of the corticosteroidDihydroquinidine barbiturate The barbiturate decreases the effect of the corticosteroidHeptabarbital The barbiturate decreases the effect of the corticosteroidHexobarbital The barbiturate decreases the effect of the corticosteroidMethohexital The barbiturate decreases the effect of the corticosteroidMethylphenobarbital The barbiturate decreases the effect of the corticosteroidPentobarbital The barbiturate decreases the effect of the corticosteroidPhenobarbital The barbiturate decreases the effect of the corticosteroidPrimidone The barbiturate decreases the effect of the corticosteroidQuinidine barbiturate The barbiturate decreases the effect of the corticosteroidSecobarbital The barbiturate decreases the effect of the corticosteroidTalbutal The barbiturate decreases the effect of the corticosteroidRifampin The enzyme inducer decreases the effect of the corticosteroidPhenytoin The enzyme inducer decreases the effect of the corticosteroidMephenytoin The enzyme inducer decreases the effect of the corticosteroidFosphenytoin The enzyme inducer decreases the effect of the corticosteroidEthotoin The enzyme inducer decreases the effect of the corticosteroidMidodrine Increased arterial pressure
Neomycin¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Not Available
|
CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸]
|
| Food Interaction |
Hydrocortisone¿¡ ´ëÇÑ Food Interaction Á¤º¸ Take with food to reduce irritation. Calcium, phosphorous, potassium, Vitamin A, C, D and zinc needs increased with long term use.
Neomycin¿¡ ´ëÇÑ Food Interaction Á¤º¸ Not Available
|
| Drug Target |
[Drug Target]
|
| Description |
Hydrocortisone¿¡ ´ëÇÑ Description Á¤º¸ The main glucocorticoid secreted by the adrenal cortex. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. [PubChem]
Neomycin¿¡ ´ëÇÑ Description Á¤º¸ A component of neomycin that is produced by Streptomyces fradiae. On hydrolysis it yields neamine and neobiosamine B. (From Merck Index, 11th ed)
|
| Drug Category |
Hydrocortisone¿¡ ´ëÇÑ Drug_Category Á¤º¸ Anti-inflammatory Agents
Neomycin¿¡ ´ëÇÑ Drug_Category Á¤º¸ Anti-Bacterial AgentsAntibiotics
|
| Smiles String Canonical |
Hydrocortisone¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CC12CCC(=O)C=C1CCC1C3CCC(O)(C(=O)CO)C3(C)CC(O)C21
Neomycin¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ NCC1OC(OC2C(N)CC(N)C(O)C2OC2OC(CO)C(OC3OC(CN)C(O)C(O)C3N)C2O)C(N)C(O)C1O
|
| Smiles String Isomeric |
Hydrocortisone¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ C[C@]12CCC(=O)C=C1CC[C@H]1[C@@H]3CC[C@](O)(C(=O)CO)[C@@]3(C)C[C@H](O)[C@H]21
Neomycin¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ NC[C@H]1O[C@H](O[C@@H]2[C@@H](N)C[C@@H](N)[C@H](O)[C@H]2O[C@@H]2O[C@H](CO)[C@@H](O[C@H]3O[C@@H](CN)[C@@H](O)[C@H](O)[C@H]3N)[C@H]2O)[C@H](N)[C@@H](O)[C@@H]1O
|
| InChI Identifier |
Hydrocortisone¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C21H30O5/c1-19-7-5-13(23)9-12(19)3-4-14-15-6-8-21(26,17(25)11-22)20(15,2)10-16(24)18(14)19/h9,14-16,18,22,24,26H,3-8,10-11H2,1-2H3/t14-,15-,16-,18+,19-,20-,21-/m0/s1
Neomycin¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C23H46N6O13/c24-2-7-13(32)15(34)10(28)21(37-7)40-18-6(27)1-5(26)12(31)20(18)42-23-17(36)19(9(4-30)39-23)41-22-11(29)16(35)14(33)8(3-25)38-22/h5-23,30-36H,1-4,24-29H2/t5-,6+,7-,8+,9-,10-,11-,12+,13-,14-,15-,16-,17-,18-,19-,20-,21-,22-,23+/m1/s1
|
| Chemical IUPAC Name |
Hydrocortisone¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ (8S,9S,10R,11S,13S,14S,17R)-11,17-dihydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-2,6,7,8,9,11,12,14,15,16-decahydro-1H-cyclopenta[a]phenanthren-3-one
Neomycin¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ (2R,3S,4R,5R,6R)-5-amino-2-(aminomethyl)-6-[(1R,2R,3S,4R,6S)-4,6-diamino-2-[(2S,3R,4S,5R)-4-[(2R,3R,4R,5S,6S)-3-amino-6-(aminomethyl)-4,5-dihydroxyoxan-2-yl]oxy-3-hydroxy-5-(hydroxymethyl)oxolan-2-yl]oxy-3-hydroxycyclohexyl]oxyoxane-3,4-diol
|
| Drug-Induced Toxicity Related Proteins |
HYDROCORTISONE ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Interleukin-8 Drug:hydrocortisone Toxicity:inflammation. [¹Ù·Î°¡±â] NEOMYCIN ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:NMDA receptor-regulated protein Drug:neomycin Toxicity:excitotoxic activation. [¹Ù·Î°¡±â]
|
|
|
 | »ç¿ëÀÚÄÁÅÙÃ÷ |
|
|
|
|
|
-
ÃÖ±ÙÁ¤º¸¼öÁ¤ÀÏ 2025-09-30
-
º» ¼öÁ¤ÀÏ Á¤º¸´Â Çã°¡Á¤º¸ ÀÌ¿ÜÀÇ ±âŸÁ¤º¸ ¼öÁ¤ÀÏÀ» ÀǹÌÇϹǷÎ, Çã°¡Á¤º¸¼öÁ¤ÀÏÀº º»¹®¿¡ Ç¥±âµÈ ³¯Â¥¸¦ ÂüÁ¶ÇϽñ⠹ٶø´Ï´Ù.
|
|
¾Ë¸² |
»ó¼¼Á¤º¸´Â ½ÄǰÀǾàǰ¾ÈÀüóÀÇ Á¦Ç°Çã°¡»çÇ×À» Åä´ë·Î ÀÛ¼ºµÇ¾úÀ¸¸ç ¿ä¾àÁ¤º¸´Â »ó¼¼Á¤º¸ ¹× ±âŸ¹®ÇåÀ» ±â¹ÝÀ¸·Î µå·°ÀÎÆ÷¿¡¼ ÆíÁýÇÑ ³»¿ëÀÔ´Ï´Ù. Á¦Ç°Çã°¡»çÇ×ÀÇ ¸ñÂ÷¿Í ´Ù¼Ò »óÀÌÇÒ ¼ö ÀÖ½À´Ï´Ù. |
|
°æ°í |
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
Ã¥ÀÓÀ» ÁöÁö ¾Ê½À´Ï´Ù. ÀÚ¼¼ÇÑ ³»¿ëÀº ¡°Ã¥ÀÓÀÇ ÇÑ°è ¹× ¹ýÀû°íÁö¡±¸¦ ÂüÁ¶ÇØ ÁֽʽÿÀ.
¹Ýµå½Ã Á¦Á¶¡¤¼öÀÔ»ç, ÆÇ¸Å»ç, ÀÇ»ç, ¾à»ç¿¡°Ô ÃÖÁ¾ÀûÀ¸·Î È®ÀÎÇϽñ⠹ٶø´Ï´Ù.
ÀüÈ: 02-3486-1061 ¤Ó À̸ÞÀÏ: webmaster@druginfo.co.kr
|
|
¾Æ·¡ÀÇ ³»¿ëÀ» Æ÷ÇÔÇÑ Àüü µ¥ÀÌÅ͸¦ º¸½Ã·Á¸é
¿©±â·Î À̵¿ÇϽñ⠹ٶø´Ï´Ù.
º´¿ë±Ý±â ¹× ƯÁ¤¿¬·É´ë ±Ý±â ¼ººÐ
|