¼¼°èÀÇ PARP(Poly ADP-Ribose Polymerase) ¾ïÁ¦Á¦ ½ÃÀå
Poly ADP-Ribose Polymerase (PARP) Inhibitors
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PARP(Poly ADP-Ribose Polymerase) ¾ïÁ¦Á¦ ¼¼°è ½ÃÀåÀº 2030³â±îÁö 349¾ï ´Þ·¯¿¡ ´ÞÇÒ Àü¸Á

2024³â¿¡ 108¾ï ´Þ·¯·Î ÃßÁ¤µÇ´Â PARP(Poly ADP-Ribose Polymerase) ¾ïÁ¦Á¦ ¼¼°è ½ÃÀåÀº 2024³âºÎÅÍ 2030³â±îÁö CAGR 21.7%·Î ¼ºÀåÇÏ¿© 2030³â¿¡´Â 349¾ï ´Þ·¯¿¡ ´ÞÇÒ °ÍÀ¸·Î ¿¹ÃøµË´Ï´Ù. ÀÌ º¸°í¼­¿¡¼­ ºÐ¼®ÇÑ ºÎ¹® Áß ÇϳªÀÎ ¼Ò¸Å ¾à±¹Àº CAGR 23.1%¸¦ ±â·ÏÇÏ¸ç ºÐ¼® ±â°£ Á¾·á½Ã¿¡´Â 233¾ï ´Þ·¯¿¡ ´ÞÇÒ °ÍÀ¸·Î ¿¹ÃøµË´Ï´Ù. º´¿ø ¾à±¹ ºÎ¹®ÀÇ ¼ºÀå·üÀº ºÐ¼® ±â°£ µ¿¾È CAGR 19.6%·Î ÃßÁ¤µË´Ï´Ù.

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¹Ì±¹ÀÇ PARP(Poly ADP-Ribose Polymerase) ¾ïÁ¦Á¦ ½ÃÀåÀº 2024³â¿¡ 29¾ï ´Þ·¯·Î ÃßÁ¤µË´Ï´Ù. ¼¼°è 2À§ °æÁ¦ ´ë±¹ÀÎ Áß±¹Àº 2030³â±îÁö 84¾ï ´Þ·¯ÀÇ ½ÃÀå ±Ô¸ð¿¡ ´ÞÇÒ °ÍÀ¸·Î ¿¹ÃøµÇ¸ç, ºÐ¼® ±â°£ÀÎ 2024-2030³â CAGRÀº 29.2%¸¦ ±â·ÏÇÒ °ÍÀ¸·Î ¿¹»óµË´Ï´Ù. ±âŸ ÁÖ¸ñÇÒ ¸¸ÇÑ Áö¿ªº° ½ÃÀåÀ¸·Î´Â ÀϺ»°ú ij³ª´Ù°¡ ÀÖ°í, ºÐ¼® ±â°£ µ¿¾È CAGRÀº °¢°¢ 17.2%¿Í 19.5%·Î ¿¹ÃøµË´Ï´Ù. À¯·´¿¡¼­´Â µ¶ÀÏÀÌ CAGR ¾à 18.2%·Î ¼ºÀåÇÒ °ÍÀ¸·Î ¿¹ÃøµË´Ï´Ù.

¼¼°èÀÇ PARP(Poly ADP-Ribose Polymerase) ¾ïÁ¦Á¦ ½ÃÀå - ÁÖ¿ä µ¿Çâ°ú ÃËÁø¿äÀÎ Á¤¸®

DNA º¹±¸ °æ·Î¸¦ Ç¥ÀûÀ¸·Î ÇÏ´Â PARP ¾ïÁ¦Á¦°¡ ¾Ï Ä¡·áÀÇ ÆÐ·¯´ÙÀÓÀ» ÀçÆíÇϰí ÀÖ½À´Ï´Ù.

PARP ¾ïÁ¦Á¦°¡ °íÇü¾Ï °ü¸®¿¡¼­ Á¤¹Ð Á¾¾çÇп¡ Çõ¸íÀ» ÀÏÀ¸Å³ ¼ö ÀÖ´Â ÀÌÀ¯´Â ¹«¾ùÀϱî?

Æú¸® ADP ¸®º¸½º ÁßÇÕÈ¿¼Ò(PARP) ¾ïÁ¦Á¦´Â ¾Ï¼¼Æ÷ÀÇ DNA º¹±¸ ¸ÞÄ¿´ÏÁòÀ» ÆÄ±«ÇÏ¿© »óµ¿°áÇÕ°á¼ÕÁõ(HRD)À» °¡Áø Á¾¾çÀ» ÇÕ¼ºÀûÀ¸·Î »ç¸ê½ÃŰ´Â Ç¥ÀûÇ×¾ÏÁ¦ÀÔ´Ï´Ù. ÀÌ °æ±¸¿ë ¾à¹°Àº ´ÜÀÏ °¡´Ú DNA Àý´Ü º¹±¸¿¡ Áß¿äÇÑ ¿ªÇÒÀ» ÇÏ´Â PARP È¿¼Ò±ºÀ» ¼±ÅÃÀûÀ¸·Î ¾ïÁ¦ÇÏ¿©, ±â´ÉÀûÀÎ BRCA1/BRCA2 ¹× ±âŸ º¹±¸ °æ·Î ´Ü¹éÁúÀÌ °á¿©µÈ ¼¼Æ÷¿¡¼­ Ä¡¸íÀûÀÎ DNA ¼Õ»óÀ» ÃàÀû½Ãŵ´Ï´Ù. ±× °á°ú, Á¤»ó¼¼Æ÷¸¦ º¸Á¸Çϸ鼭 Á¾¾ç¼¼Æ÷¸¦ ¼±ÅÃÀûÀ¸·Î »ç¸ê½Ãų ¼ö ÀÖ¾î ¸ÂÃãÇü ÀÇ·á¿¡ Å« ÁøÀüÀ» °¡Á®´Ù ÁÙ ¼ö ÀÖ½À´Ï´Ù. ´çÃÊ PARP ¾ïÁ¦Á¦´Â BRCA º¯ÀÌ ³­¼Ò¾ÏÀ» ÀûÀÀÁõÀ¸·Î ½ÂÀÎ ¹Þ¾ÒÀ¸³ª, ÇöÀç´Â À¯¹æ¾Ï, Àü¸³¼±¾Ï, ÃéÀå¾Ï, Àڱ󻸷¾Ï µîÀ¸·Î ÀûÀÀÁõÀ» È®´ëÇϰí ÀÖ½À´Ï´Ù. ½ÂÀÎµÈ ÁÖ¿ä ¾àÁ¦¿¡´Â ¿Ã¶óÆÄ¸³(¸°ÆÄÀÚ), ´Ï¶óÆÄ¸³(Á¦ÁÙ¶ó), ·çÄ«ÆÄ¸³(·çºê¶óÄ«), Ÿ¶óÁ¶ÆÄ¸³(Ÿ¸£Á¨³ª) µîÀÌ ÀÖÀ¸¸ç, °¢°¢ °íÀ¯ÇÑ ¾àµ¿ÇÐ, µ¶¼º ÇÁ·ÎÆÄÀÏ, Åõ¾à ÇÁ·ÎÅäÄÝÀ» °¡Áö°í ÀÖ½À´Ï´Ù. ÀÌ·¯ÇÑ Ä¡·á¹ýÀº ƯÈ÷ HRD ¾ç¼º Á¾¾ç ȯÀÚ¸¦ ´ë»óÀ¸·Î 1Â÷ Ä¡·á¿Í À¯Áö¿ä¹ý ¸ðµÎ¿¡¼­ Ä¡·áÀÇ ±âÁØÀ» ÀçÁ¤ÀÇÇϰí ÀÖ½À´Ï´Ù. PARP ¾ïÁ¦Á¦ÀÇ Ä¡·áÀû ÀåÁ¡Àº ±âÁ¸ È­Çпä¹ýÀ¸·Î ÃæºÐÈ÷ Ä¡·áÇÒ ¼ö ¾ø¾ú´ø À¯ÀüÀûÀ¸·Î Á¤ÀÇµÈ Á¾¾ç ¾ÆÇü¿¡ ´ëÀÀÇÒ ¼ö ÀÖ´Ù´Â Á¡ÀÔ´Ï´Ù. °æ±¸ Åõ¿©¿Í ¿ì¼öÇÑ µ¶¼º ÇÁ·ÎÆÄÀÏÀº ȯÀÚÀÇ ¼øÀÀµµ¸¦ ´õ¿í ³ô¿© Á¾¾ç Æ÷Æ®Æú¸®¿À¿¡¼­ ¸Å·ÂÀûÀÎ ¼±ÅÃÀÌ µÉ ¼ö ÀÖ½À´Ï´Ù.

PARP ¾ïÁ¦Á¦ÀÇ ¼¼°è º¸±ÞÀ» ÁÖµµÇϰí ÀÖ´Â ¾ÏÁ¾°ú ȯÀÚ±ºÀº?

³­¼Ò¾ÏÀº ¿©ÀüÈ÷ PARP ¾ïÁ¦Á¦ Ä¡·áÀÇ ÁÖ¿ä ÀûÀÀÁõÀÔ´Ï´Ù. PARP ¾ïÁ¦Á¦¸¦ ÀÌ¿ëÇÑ À¯Áö¿ä¹ýÀº BRCA À¯ÀüÀÚ º¯ÀÌ ¹× ±¤¹üÀ§ÇÑ HRD ½Ã±×´Ïó¸¦ °¡Áø ȯÀÚÀÇ ¹«ÁøÇà »ýÁ¸±â°£À» ÃÖÀü¼± ¹× Àç¹ß ȯÀÚ ¸ðµÎ¿¡¼­ À¯ÀÇÇÏ°Ô ¿¬Àå½ÃÄ×½À´Ï´Ù. SOLO-1, PRIMA, ARIEL3 µîÀÇ ÀÓ»ó 3»ó ½ÃÇèÀ» ¹ÙÅÁÀ¸·Î ¾à»ç¹ý ½ÂÀÎÀ» È®´ëÇÏ¿´½À´Ï´Ù. ÀÌ·¯ÇÑ ÀÓ»ó½ÃÇèÀ» ÅëÇØ BRCA À¯ÀüÀÚ º¯ÀÌ ¹× HRD ¾ç¼ºÀÎ ÇÏÀ§ ±×·ì¿¡¼­ PARP ¾ïÁ¦Á¦ÀÇ À¯¿ë¼ºÀÌ °ËÁõµÇ¾î ÀÓ»óÀû À¯¿ë¼ºÀÌ È®´ëµÇ¾ú½À´Ï´Ù. À¯¹æ¾Ï, ƯÈ÷ »ý½Ä¼¼Æ÷ °è¿­ÀÇ BRCA À¯ÀüÀÚ º¯À̰¡ ÀÖ´Â »ïÁßÀ½¼º Á¾¾ç°ú HER2 À½¼º Á¾¾ç¿¡¼­ PARP ¾ïÁ¦Á¦´Â È­Çпä¹ý ÈÄ ´Üµ¶¿ä¹ý ¶Ç´Â º´¿ë¿ä¹ýÀ¸·Î ÁöÁö¹Þ°í ÀÖ½À´Ï´Ù. OlympiAD ½ÃÇè°ú EMBRACA ½ÃÇèÀº ±× È¿´ÉÀ» µÞ¹ÞħÇÏ´Â È®½ÇÇÑ Áõ°Å¸¦ Á¦°øÇß°í, ÀüÀÌ Ä¡·á °æ·Î¿¡ ÅëÇյǾú½À´Ï´Ù. ÀüÀ̼º °Å¼¼ÀúÇ×¼º Àü¸³¼±¾Ï(mCRPC)ÀÇ °æ¿ì, ƯÁ¤ DNA ¼Õ»ó º¹±¸(DDR) À¯ÀüÀÚ º¯À̰¡ Àִ ȯÀÚ¿¡°Ô ¿Ã¶óÆÄ¸³°ú ·çÄ«ÆÄ¸³°ú °°Àº ¾à¹°ÀÌ ½ÂÀεǸ鼭 ÀÓ»óÀû ¿µÇâ·ÂÀÌ ´õ¿í È®´ëµÇ°í ÀÖ½À´Ï´Ù. ÃéÀå¾ÏÀº ±×µ¿¾È ¿¹Èİ¡ ÁÁÁö ¾Ê¾Æ Ä¡·á ¿É¼ÇÀÌ Á¦ÇÑÀûÀ̾úÀ¸³ª, PARP ¾ïÁ¦Á¦ÀÇ »õ·Î¿î °³Ã´Áö·Î ¶°¿À¸£°í ÀÖ½À´Ï´Ù. POLO ½ÃÇèÀº BRCA µ¹¿¬º¯ÀÌ Á¾¾ç ȯÀÚ¸¦ À§ÇÑ À¯Áö¿ä¹ýÀ¸·Î¼­ ¿Ã¶óÆÄ¸³ÀÇ À¯¿ë¼ºÀ» ÀÔÁõÇÏ¿© ÀÌ ¾Ç¼ºÁ¾¾ç¿¡ ÀÖ¾î Áß¿äÇÑ µ¹ÆÄ±¸¸¦ ¸¶·ÃÇÏ¿´½À´Ï´Ù. ¶ÇÇÑ, DNA º¹±¸ ÀÌ»óÀÌ Á¸ÀçÇÏ´Â Àڱ󻸷¾Ï, ´ã°ü¾Ï, ¼Ò¼¼Æ÷Æó¾Ï¿¡ ´ëÇÑ PARPÀÇ È¿´ÉÀÌ ½ÇÁ¦ Áõ°Å¿Í ¹Ù½ºÄÏ ½ÃÇèÀ» ÅëÇØ °ËÅäµÇ°í ÀÖ½À´Ï´Ù.

ÀÓ»ó Àü·«°ú º´¿ë¿ä¹ýÀº PARP ¾ïÁ¦Á¦ÀÇ À¯¿ë¼ºÀ» ¾î¶»°Ô ³ôÀ̰í Àִ°¡?

PARP ¾ïÁ¦Á¦¸¦ µÑ·¯½Ñ ÀÓ»ó Àü·«Àº ºü¸£°Ô ÁøÈ­Çϰí ÀÖÀ¸¸ç, ¸é¿ª°ü¹®¾ïÁ¦Á¦(ICI), Ç÷°ü½Å»ý¾ïÁ¦Á¦, È­Çпä¹ý°úÀÇ º´¿ë¿ä¹ýÀ» Æò°¡Çϱâ À§ÇÑ ÀÓ»ó½ÃÇèÀÌ ÁøÇà ÁßÀÔ´Ï´Ù. ÀüÀÓ»ó µ¥ÀÌÅÍ´Â PARP ¾ïÁ¦°¡ cGAS-STING °æ·Î¸¦ Ȱ¼ºÈ­ÇÏ¿© Á¾¾çÀÇ ¸é¿ª¿ø¼ºÀ» ³ôÀ̰í PD-1/PD-L1 Â÷´ÜÀÇ È¿´ÉÀ» ³ôÀδٴ °ÍÀ» ½Ã»çÇÕ´Ï´Ù. MEDIOLA¿Í TOPACIO¿Í °°Àº ÀÓ»ó½ÃÇèÀº À¯¹æ¾Ï°ú ³­¼Ò¾Ï¿¡¼­ ÀÌ·¯ÇÑ ½Ã³ÊÁö È¿°ú¸¦ Æò°¡Çϰí ÀÖ½À´Ï´Ù. º£¹Ù½ÃÁÖ¸¿°ú °°Àº VEGF ¾ïÁ¦Á¦¿ÍÀÇ º´¿ë¿ä¹ýÀº ƯÈ÷ ¹é±ÝÁ¦Á¦ ¹Î°¨¼º ³­¼Ò¾Ï¿¡¼­ À¯¸ÁÇÑ °á°ú¸¦ º¸À̰í ÀÖ½À´Ï´Ù. PAOLA-1 ½ÃÇè¿¡¼­ ¿Ã¶óÆÄ¸³°ú º£¹Ù½ÃÁÖ¸¿ÀÇ º´¿ë¿ä¹ýÀÌ HRD ¾ç¼º ȯÀÚÀÇ PFS¸¦ À¯ÀÇÇÏ°Ô ¿¬ÀåÇÏ´Â °ÍÀ¸·Î ³ªÅ¸³ª BRCA º¯ÀÌÁ¾¾ç ¿ÜÀÇ ´Ù¸¥ ¾ÏÁ¾¿¡¼­ PARP ¾ïÁ¦Á¦ »ç¿ëÀ» ÁöÁöÇÏ´Â ±Ù°Å°¡ µÇ¾ú½À´Ï´Ù. ´Ù¸¥ ½ÃÇè¿¡¼­´Â ¹é±Ý Á¦Á¦ ¹ÝÀÀ ÈÄ PARP ¾ïÁ¦Á¦¸¦ »ç¿ëÇϰųª, Ź»ê°è È­Çпä¹ý°ú µ¿½Ã¿¡ »ç¿ëÇÔÀ¸·Î½á ÀÓ»óÀû À¯¿ë¼ºÀ» ÃÖÀûÈ­ÇÏ´Â ½ÃÄö½Ì Àü·«ÀÌ °ËÅäµÇ°í ÀÖ½À´Ï´Ù. ¹ÙÀÌ¿À¸¶Ä¿ °³¹ßµµ ÁøÇà ÁßÀÔ´Ï´Ù. BRCA1/2 ¿Ü¿¡µµ ATM, CHEK2, RAD51, PALB2ÀÇ º¯È­°¡ PARP °¨¼ö¼º ¿¹Ãø ¸¶Ä¿·Î °ËÁõµÇ°í ÀÖ½À´Ï´Ù. À¯Àüü ºÒ¾ÈÁ¤¼º Á¡¼ö¸¦ ÀÌ¿ëÇÑ HRD °Ë»ç°¡ ÀÓ»ó ¿öÅ©Ç÷ο쿡 ÅëÇյǾî Àû°Ý ȯÀÚ¸¦ º¸´Ù Á¤È®ÇÏ°Ô ½Äº°ÇÒ ¼ö ÀÖµµ·Ï Çϰí ÀÖ½À´Ï´Ù. µ¿¹ÝÁø´Ü¾àÀº Ä¡·á¹ýÀÇ ½ÂÀΰú ÇÔ²² ÁøÈ­Çϰí ÀÖÀ¸¸ç, ¾à¹°ÀÇ °³¹ß°ú ºÐÀÚ°Ë»ç ÀÎÇÁ¶ó¸¦ ÀÏÄ¡½Ã۰í ÀÖ½À´Ï´Ù.

PARP ¾ïÁ¦Á¦ÀÇ ¼¼°è ¼ºÀåÀ» ÃËÁøÇÏ´Â ½ÃÀå ÃËÁø¿äÀÎÀº ¹«¾ùÀΰ¡?

PARP ¾ïÁ¦Á¦ ½ÃÀåÀÇ ¼ºÀåÀº Á¤¹Ð Á¾¾çÇÐÀÇ È®´ë, ¹ÙÀÌ¿À¸¶Ä¿¿¡ ±â¹ÝÇÑ È¯ÀÚ °èÃþÈ­, BRCA ¾ç¼º ȯÀÚ Áõ°¡ µî ¿©·¯ °¡Áö ¿äÀÎÀÌ º¹ÇÕÀûÀ¸·Î ÀÛ¿ëÇÏ¿© ÀÌ·ç¾îÁö°í ÀÖ½À´Ï´Ù. °¡Àå Å« ¿øµ¿·Â Áß Çϳª´Â ¸ÂÃãÇü ¾Ï Ä¡·á·ÎÀÇ ÆÐ·¯´ÙÀÓ ÀüȯÀÔ´Ï´Ù. Â÷¼¼´ë ¿°±â¼­¿­ºÐ¼®(NGS)ÀÌ ¾Ï Ä¡·áÀÇ Ç¥ÁØÀ¸·Î ÀÚ¸® ÀâÀ¸¸é¼­ HRD °ü·Ã µ¹¿¬º¯À̸¦ °¡Áø ȯÀÚµéÀÌ ´õ ¸¹ÀÌ ¹ß°ßµÇ°í, PARP ¾ïÁ¦Á¦ ½ÃÀåÀÌ È®´ëµÇ°í ÀÖ½À´Ï´Ù. ƯÈ÷ ³­¼Ò¾Ï, Àü¸³¼±¾Ï µî Àϼ±¿¡¼­ µ¶¼ºÀ» ÃÖ¼ÒÈ­ÇÑ À¯Áö¿ä¹ý¿¡ ´ëÇÑ ¼ö¿ä°¡ Áõ°¡Çϸ鼭 Àϼ±¿¡¼­ÀÇ µµÀÔÀÌ °¡¼ÓÈ­µÇ°í ÀÖ½À´Ï´Ù. ¶ÇÇÑ, µ¿¹ÝÁø´ÜÁ¦ ¹× ¹ÙÀÌ¿À¸¶Ä¿ ±â¹Ý ó¹æ¿¡ ´ëÇÑ ÁöºÒÀÚÀÇ Áö¿øÀÌ Áõ°¡ÇÔ¿¡ µû¶ó, »óȯ À庮ÀÌ ³·¾ÆÁ® Áö¿ª ¾Ï Áø·á ¹× ½ÅÈï ÀÇ·á ½Ã½ºÅÛ¿¡¼­ Æø³Ð°Ô äÅÃµÉ ¼ö ÀÖ°Ô µÇ¾ú½À´Ï´Ù.

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Global Poly ADP-Ribose Polymerase (PARP) Inhibitors Market to Reach US$34.9 Billion by 2030

The global market for Poly ADP-Ribose Polymerase (PARP) Inhibitors estimated at US$10.8 Billion in the year 2024, is expected to reach US$34.9 Billion by 2030, growing at a CAGR of 21.7% over the analysis period 2024-2030. Retail Pharmacies, one of the segments analyzed in the report, is expected to record a 23.1% CAGR and reach US$23.3 Billion by the end of the analysis period. Growth in the Hospital Pharmacies segment is estimated at 19.6% CAGR over the analysis period.

The U.S. Market is Estimated at US$2.9 Billion While China is Forecast to Grow at 29.2% CAGR

The Poly ADP-Ribose Polymerase (PARP) Inhibitors market in the U.S. is estimated at US$2.9 Billion in the year 2024. China, the world's second largest economy, is forecast to reach a projected market size of US$8.4 Billion by the year 2030 trailing a CAGR of 29.2% over the analysis period 2024-2030. Among the other noteworthy geographic markets are Japan and Canada, each forecast to grow at a CAGR of 17.2% and 19.5% respectively over the analysis period. Within Europe, Germany is forecast to grow at approximately 18.2% CAGR.

Global Poly ADP-Ribose Polymerase (PARP) Inhibitors Market - Key Trends & Drivers Summarized

Targeting DNA Repair Pathways: How PARP Inhibitors Are Reshaping Cancer Therapy Paradigms

Why Are PARP Inhibitors Revolutionizing Precision Oncology in Solid Tumor Management?

Poly ADP-ribose polymerase (PARP) inhibitors are a class of targeted cancer therapies that disrupt DNA repair mechanisms in cancer cells, leading to synthetic lethality in tumors with homologous recombination deficiencies (HRD). These oral agents selectively inhibit the PARP enzyme family-key players in repairing single-strand DNA breaks-thereby allowing lethal DNA damage to accumulate in cells lacking functional BRCA1/BRCA2 or other repair pathway proteins. The result is selective tumor cell death while sparing normal cells, offering a significant advancement in personalized medicine. Initially approved for BRCA-mutated ovarian cancer, PARP inhibitors have expanded into indications including breast, prostate, pancreatic, and endometrial cancers. Major approved agents include olaparib (Lynparza), niraparib (Zejula), rucaparib (Rubraca), and talazoparib (Talzenna), each with unique pharmacokinetics, toxicity profiles, and dosing protocols. These therapies have redefined treatment standards in both first-line and maintenance settings, particularly for patients with HRD-positive tumors. The therapeutic advantage of PARP inhibitors lies in their capacity to address genetically defined tumor subtypes that were previously underserved by conventional chemotherapy. Their oral administration and favorable toxicity profiles further enhance patient compliance, making them an attractive option in oncology portfolios.

Which Cancer Types and Patient Populations Are Driving the Adoption of PARP Inhibitors Globally?

Ovarian cancer remains the leading indication for PARP inhibitor therapy. In both frontline and recurrence settings, maintenance therapy with PARP inhibitors has significantly extended progression-free survival in patients with BRCA mutations or broader HRD signatures. Regulatory approvals have been expanded based on Phase III trials such as SOLO-1, PRIMA, and ARIEL3. These trials have validated the benefit of PARP inhibitors across BRCA-mutated and HRD-positive subgroups, broadening their clinical utility. In breast cancer, particularly triple-negative and HER2-negative tumors with germline BRCA mutations, PARP inhibitors have gained traction as monotherapy or combination therapy following chemotherapy. The OlympiAD and EMBRACA trials have provided robust evidence supporting their efficacy, leading to their integration into metastatic treatment pathways. In metastatic castration-resistant prostate cancer (mCRPC), agents like olaparib and rucaparib have been approved for patients with specific DNA damage repair (DDR) gene alterations, further expanding the clinical footprint of these agents. Pancreatic cancer, historically associated with poor prognosis and limited treatment options, has emerged as a new frontier for PARP inhibitors. The POLO trial demonstrated the utility of olaparib as a maintenance therapy for patients with BRCA-mutated tumors, representing a significant breakthrough in this notoriously aggressive malignancy. Additionally, real-world evidence and basket trials are exploring PARP efficacy in endometrial, bile duct, and small cell lung cancers where DNA repair defects are present.

How Are Clinical Strategies and Combination Therapies Enhancing PARP Inhibitor Utility?

The clinical strategy around PARP inhibitors is evolving rapidly with ongoing trials assessing their use in combination with immune checkpoint inhibitors (ICIs), anti-angiogenic agents, and chemotherapy. Preclinical data suggest that PARP inhibition increases tumor immunogenicity by activating cGAS-STING pathways, thereby enhancing the efficacy of PD-1/PD-L1 blockade. Trials like MEDIOLA and TOPACIO are evaluating this synergy in breast and ovarian cancers. Combination with VEGF inhibitors such as bevacizumab has shown promising outcomes, particularly in platinum-sensitive ovarian cancer. The PAOLA-1 trial demonstrated that olaparib plus bevacizumab extended PFS significantly in HRD-positive patients, supporting the use of PARP inhibitors beyond BRCA-mutated tumors. Additionally, studies are investigating sequencing strategies-using PARP inhibitors after platinum response or concurrently with taxane-based chemotherapy-to optimize clinical benefit. Biomarker development is also advancing. Beyond BRCA1/2, alterations in ATM, CHEK2, RAD51, and PALB2 are being validated as predictive markers of PARP sensitivity. HRD testing using genomic instability scores is being integrated into clinical workflows to identify eligible patients more accurately. Companion diagnostics are co-evolving with therapy approvals, aligning drug deployment with molecular testing infrastructure.

What Market Drivers Are Propelling the Global Growth of PARP Inhibitors?

The growth in the PARP inhibitors market is driven by multiple intersecting forces including precision oncology expansion, biomarker-based patient stratification, and increasing prevalence of BRCA-tested patients. One of the foremost drivers is the paradigm shift toward personalized cancer therapy. As next-generation sequencing (NGS) becomes standard practice in oncology, more patients are being identified with HRD-related mutations, expanding the addressable market for PARP inhibitors. The demand for maintenance therapies with minimal toxicity is accelerating uptake in frontline settings, particularly in ovarian and prostate cancers. Additionally, growing payer support for companion diagnostics and biomarker-guided prescribing is reducing reimbursement hurdles, enabling broader adoption across community oncology practices and emerging healthcare systems.

Regulatory support is also robust, with breakthrough therapy designations, fast-track approvals, and international regulatory harmonization accelerating market entry. Emerging economies in Asia-Pacific and Latin America are incorporating PARP inhibitors into national cancer control strategies, driven by rising awareness of BRCA testing and inclusion in treatment guidelines. As combination regimens, earlier-line indications, and pan-cancer biomarker approvals progress through pipelines, the commercial outlook for PARP inhibitors is poised for sustained growth. Their expanding clinical versatility, oral delivery format, and synergy with other targeted agents make them central to the future of oncology therapeutics.

SCOPE OF STUDY:

The report analyzes the Poly ADP-Ribose Polymerase (PARP) Inhibitors market in terms of units by the following Segments, and Geographic Regions/Countries:

Segments:

Distribution Channel (Retail Pharmacies, Hospital Pharmacies, Online Distribution Channel); End-Use (Ovarian Cancer End-Use, Breast Cancer End-Use, Other End-Uses)

Geographic Regions/Countries:

World; United States; Canada; Japan; China; Europe (France; Germany; Italy; United Kingdom; Spain; Russia; and Rest of Europe); Asia-Pacific (Australia; India; South Korea; and Rest of Asia-Pacific); Latin America (Argentina; Brazil; Mexico; and Rest of Latin America); Middle East (Iran; Israel; Saudi Arabia; United Arab Emirates; and Rest of Middle East); and Africa.

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TABLE OF CONTENTS

I. METHODOLOGY

II. EXECUTIVE SUMMARY

III. MARKET ANALYSIS

IV. COMPETITION

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