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DNA Repair Drugs
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DNA º¹±¸ ¾à¹° ¼¼°è ½ÃÀåÀº 2030³â±îÁö ¹Ì±¹¿¡¼­ 195¾ï ´Þ·¯¿¡ ´ÞÇÒ Àü¸Á

2024³â¿¡ 83¾ï ´Þ·¯·Î ÃßÁ¤µÇ´Â DNA º¹±¸ ¾à¹° ¼¼°è ½ÃÀåÀº ºÐ¼® ±â°£ÀÎ 2024-2030³â¿¡ CAGR 15.2%·Î ¼ºÀåÇÏ¿© 2030³â¿¡´Â 195¾ï ´Þ·¯¿¡ ´ÞÇÒ °ÍÀ¸·Î ¿¹ÃøµË´Ï´Ù. ÀÌ º¸°í¼­¿¡¼­ ºÐ¼®ÇÑ ºÎ¹® Áß ÇϳªÀΠǥÀû¿ä¹ýÀº CAGR 17.2%¸¦ ±â·ÏÇÏ¸ç ºÐ¼® ±â°£ Á¾·á±îÁö 85¾ï ´Þ·¯¿¡ ´ÞÇÒ °ÍÀ¸·Î ¿¹»óµË´Ï´Ù. È£¸£¸ó¿ä¹ý ºÐ¾ßÀÇ ¼ºÀå·üÀº ºÐ¼® ±â°£ µ¿¾È CAGR 11.8%·Î ÃßÁ¤µË´Ï´Ù.

¹Ì±¹ ½ÃÀåÀº 22¾ï ´Þ·¯·Î ÃßÁ¤, Áß±¹Àº CAGR 14.2%·Î ¼ºÀå ¿¹Ãø

¹Ì±¹ÀÇ DNA º¹±¸ ¾à¹° ½ÃÀåÀº 2024³â¿¡ 22¾ï ´Þ·¯·Î ÃßÁ¤µË´Ï´Ù. ¼¼°è 2À§ °æÁ¦ ´ë±¹ÀÎ Áß±¹Àº ºÐ¼® ±â°£ÀÎ 2024-2030³â CAGR 14.2%·Î ÃßÁ¤µÇ¸ç, 2030³â±îÁö 30¾ï ´Þ·¯ÀÇ ½ÃÀå ±Ô¸ð¿¡ ´ÞÇÒ °ÍÀ¸·Î ¿¹ÃøµË´Ï´Ù. ±âŸ ÁÖ¸ñÇÒ ¸¸ÇÑ Áö¿ªº° ½ÃÀåÀ¸·Î´Â ÀϺ»°ú ij³ª´Ù°¡ ÀÖ°í, ºÐ¼® ±â°£ µ¿¾È CAGRÀº °¢°¢ 14.3%¿Í 12.9%·Î ¿¹ÃøµË´Ï´Ù. À¯·´¿¡¼­´Â µ¶ÀÏÀÌ CAGR 10.9%·Î ¼ºÀåÇÒ °ÍÀ¸·Î ¿¹ÃøµË´Ï´Ù.

¼¼°èÀÇ DNA º¹±¸ ¾à¹° ½ÃÀå - ÁÖ¿ä µ¿Çâ°ú ÃËÁø¿äÀÎ Á¤¸®

DNA º¹±¸ ¸ÞÄ¿´ÏÁòÀ» Ç¥ÀûÀ¸·Î »ï´Â °ÍÀÌ ¾Ï Ä¡·áÀÇ ÆÐ·¯´ÙÀÓÀ» ÀçÁ¤ÀÇÇÒ ¼ö ÀÖÀ»±î?

DNA º¹±¸ ¸ÞÄ¿´ÏÁò¿¡ ´ëÇÑ ¿¬±¸´Â Ä¡·áÀûÀ¸·Î ÀÌ¿ë °¡´ÉÇÑ ¾Ï¼¼Æ÷ÀÇ Ãë¾à¼ºÀ» ¹àÇô³¿À¸·Î½á Á¾¾çÇп¡ Çõ¸íÀ» ÀÏÀ¸Ä×½À´Ï´Ù. À¯Àüü ¹«°á¼º À¯Áö¿¡ °ü¿©Çϴ ƯÁ¤ È¿¼Ò³ª °æ·Î¸¦ Ç¥ÀûÀ¸·Î »ï´Â DNA º¹±¸ ¾à¹°Àº ÀÌ·¯ÇÑ º¯È­ÀÇ ÃÖÀü¼±¿¡ ÀÖ½À´Ï´Ù. ¾Ï¼¼Æ÷´Â ÁÖ¿ä º¹±¸ °æ·ÎÀÇ °áÇÔÀ¸·Î ÀÎÇØ ´ëü DNA º¹±¸ ¸ÞÄ¿´ÏÁò¿¡ Å©°Ô ÀÇÁ¸ÇÏ´Â °æ¿ì°¡ ¸¹½À´Ï´Ù. ÇÕ¼º Ä¡»ç·Î ¾Ë·ÁÁø ÀÌ °³³äÀº PARP(Æú¸® ADP ¸®º¸½º ÁßÇÕÈ¿¼Ò) ¾ïÁ¦Á¦¿Í °°ÀÌ FDA ½ÂÀÎÀ» ¹ÞÀº ¿©·¯ ¾à¹°ÀÇ ±âÃʰ¡ µÇ¾úÀ¸¸ç, BRCA µ¹¿¬º¯ÀÌ ³­¼Ò¾Ï, À¯¹æ¾Ï, ÃéÀå¾Ï, Àü¸³¼±¾Ï Ä¡·á¿¡ Ź¿ùÇÑ È¿´ÉÀ» º¸À̰í ÀÖ½À´Ï´Ù. DNA º¹±¸ ¾ïÁ¦Á¦ÀÇ À¯¸Á¼ºÀº Á¤»ó ¼¼Æ÷¸¦ º¸Á¸Çϸ鼭 Á¾¾ç ¼¼Æ÷¸¦ ¼±ÅÃÀûÀ¸·Î »ç¸ê½ÃŰ´Â ´É·Â¿¡ ÀÖÀ¸¸ç, È­Çпä¹ý¿¡¼­ ÈçÈ÷ ¹ß»ýÇϴ ǥÀû ¿Ü µ¶¼ºÀ» °¨¼Ò½Ã۴µ¥ ÀÖ½À´Ï´Ù. PARP ¿Ü¿¡µµ ATM, ATR, DNA-PK, CHK1/2, POLQ µî DNA ¼Õ»ó¿¡ ´ëÇÑ ¼¼Æ÷ ¹ÝÀÀ¿¡ Áß¿äÇÑ ¿ªÇÒÀ» ÇÏ´Â ´Ù¾çÇÑ Ç¥ÀûµéÀ» Àû±ØÀûÀ¸·Î Ž»öÇϰí ÀÖ½À´Ï´Ù. ÀÌ·¯ÇÑ »õ·Î¿î Ä¡·á¹ýÀº ¸é¿ª¿ä¹ý, ¹æ»ç¼±¿ä¹ý, ÀüÅëÀû È­Çпä¹ý°ú ÇÔ²² ´Üµ¶¿ä¹ý ¹× º´¿ë¿ä¹ýÀ¸·Î Æò°¡¹Þ°í ÀÖ½À´Ï´Ù. DNA º¹±¸¸¦ Ç¥ÀûÀ¸·Î ÇÏ´Â Ä¡·á¹ýÀÇ Á¤È®¼º°ú °³º°È­·Î ÀÎÇØ °³ÀÎÀÇ À¯Àüü ÇÁ·ÎÆÄÀÏ¿¡ ¸ÂÃá º¸´Ù È¿°úÀûÀÎ Ä¡·á Àü·«ÀÌ °¡´ÉÇØÁ³½À´Ï´Ù. µû¶ó¼­ ¹ÙÀÌ¿À¸¶Ä¿ Áß½ÉÀÇ ¾à¹° °³¹ßÀº ÀÌ ºÐ¾ß¿¡¼­ ÇÙ½ÉÀûÀÎ ¿ªÇÒÀ» Çϰí ÀÖÀ¸¸ç, µ¿¹ÝÁø´ÜÀÌ °¡Àå È¿°úÀûÀÏ °ÍÀ¸·Î ±â´ëµÇ´Â ȯÀÚ¸¦ ½Äº°ÇÏ´Â µ¥ Ȱ¿ëµÇ°í ÀÖ½À´Ï´Ù. DNA ¼Õ»ó ¹ÝÀÀ(DDR) ³×Æ®¿öÅ©¿¡ ´ëÇÑ ÀÌÇØ°¡ ±í¾îÁü¿¡ µû¶ó DNA º¹±¸ ¾à¹°Àº ¾Ï Ä¡·á ¹æ¹ýÀ» ÀçÁ¤ÀÇÇϰí ÀÖ½À´Ï´Ù. Áï, ¸¸´É ¸ðµ¨¿¡¼­ °íµµ·Î Ç¥ÀûÈ­µÈ ±âÀü ƯÀÌÀû Á¢±Ù¹ýÀ¸·Î ÀüȯÇÏ¿© ¾ÏÇÐÀÇ »õ·Î¿î ½Ã´ë¸¦ ¸ÂÀÌÇϰí ÀÖ½À´Ï´Ù.

À¯ÀüüÇÐ ¹× ¹ÙÀÌ¿À¸¶Ä¿ °úÇÐÀÇ ¹ßÀüÀº ÀǾàǰ °³¹ßÀ» ¾î¶»°Ô ÃËÁøÇϰí Àִ°¡?

À¯ÀüüÇÐ, ½ÃÄö½Ì, ºÐÀÚÁø´ÜÀÇ ±â¼úÀû ¹ßÀüÀº Á¾¾çÀÇ DNA º¹±¸ °á¼ÕÀ» Á¤È®ÇÏ°Ô ½Äº°ÇÒ ¼ö ÀÖ°ÔÇÔÀ¸·Î½á DNA º¹±¸ ¾à¹°ÀÇ °³¹ß°ú ÀÓ»ó Àû¿ëÀ» ÃËÁøÇϰí ÀÖ½À´Ï´Ù. BRCA1/2, ATM, PALB2, ±âŸ »óµ¿ ÀçÁ¶ÇÕ º¹±¸(HRR) ¹× ºÒÀÏÄ¡ º¹±¸(MMR) °æ·ÎÀÇ ±¸¼º¿ä¼Ò¿Í °°Àº À¯ÀüÀÚÀÇ µ¹¿¬º¯À̸¦ °ËÃâÇϱâ À§ÇØ ÇöÀç ÇÏÀ̽º·çDz ½ÃÄö½Ì ¹× Â÷¼¼´ë ½ÃÄö½Ì(NGS) Ç÷§ÆûÀÌ ³Î¸® »ç¿ëµÇ°í ÀÖ½À´Ï´Ù. ÀÌ·¯ÇÑ ÀλçÀÌÆ®¸¦ ÅëÇØ ÀÓ»óÀÇ¿Í ¿¬±¸ÀÚµéÀº À¯ÀüÀû ±¸¼º¿¡ µû¶ó ȯÀÚ¸¦ °èÃþÈ­ÇÏ¿© Ä¡·á ¹ÝÀÀÀ» º¸´Ù Á¤È®ÇÏ°Ô ¿¹ÃøÇÒ ¼ö ÀÖ½À´Ï´Ù. ¶ÇÇÑ, "BRCAness", »óµ¿°áÇÕ°á¼Õ(HRD) Á¡¼ö µî »õ·Î¿î À¯Àüü ½Ã±×´ÏóÀÇ ¹ß°ßÀ¸·Î DNA º¹±¸ ¾à¹°ÀÇ Àû°Ý¼º ±âÁØÀº »ý½Ä¼¼Æ÷ °è¿­ÀÇ BRCA À¯ÀüÀÚ º¯ÀÌ¿¡¸¸ ±¹ÇѵÇÁö ¾Ê°í È®´ëµÇ°í ÀÖ½À´Ï´Ù. ¼øÈ¯ Á¾¾ç DNA(ctDNA)¸¦ °ËÃâÇÏ´Â ¾×ü »ý°Ëµµ ½Ç½Ã°£À¸·Î Ä¡·á ¹ÝÀÀ¼º°ú ÀúÇ×¼ºÀ» ¸ð´ÏÅ͸µÇÏ´Â ÃÖ¼Òħ½ÀÀû µµ±¸·Î °¢±¤¹Þ°í ÀÖ½À´Ï´Ù. ¹ÙÀÌ¿À¸¶Ä¿¿¡ ±â¹ÝÇÑ ÀǾàǰ °³¹ßÀº Á¦¾àȸ»çµé¿¡°Ô Áß¿äÇÑ Àü·«ÀÌ µÇ°í ÀÖÀ¸¸ç, dzºÎÇÑ È¯ÀÚ±º°ú ´õ ³ôÀº ¼º°ø È®·üÀ» °¡Áø º¸´Ù ½º¸¶Æ®ÇÑ ÀÓ»ó½ÃÇèÀ» ¼³°èÇÏ´Â µ¥ µµ¿òÀ» ÁÖ°í ÀÖ½À´Ï´Ù. ¶ÇÇÑ, CRISPR-Cas9 À¯ÀüÀÚ ÆíÁýÀº ƯÁ¤ DNA º¹±¸ À¯ÀüÀÚÀÇ ¿ªÇÒ°ú ¾Ï ÁøÇà¿¡ ´ëÇÑ ±â¿©µµ¸¦ ´õ Àß ÀÌÇØÇϱâ À§ÇØ ÀüÀÓ»ó ¸ðµ¨¿¡¼­ »ç¿ëµÇ¾î »õ·Î¿î Ä¡·á Ç¥Àû ¹ß±¼ÀÇ ±æÀ» ¿­¾îÁÖ°í ÀÖ½À´Ï´Ù. ¶ÇÇÑ, ÀνǸ®ÄÚ ¸ðµ¨¸µ°ú AI ±â¹Ý ½Å¾à°³¹ß Ç÷§ÆûÀº ´õ ³ôÀº ¼±Åüº°ú È¿´ÉÀ» °¡Áø ÀúºÐÀÚ ¾ïÁ¦Á¦ ¹ß±¼À» °¡¼ÓÈ­Çϰí ÀÖ½À´Ï´Ù. ÀÌ·¯ÇÑ ±â¼úÀû ½Ã³ÊÁö È¿°ú´Â ¾à¹° ¼³°è¸¦ Á¤±³È­ÇÒ »Ó¸¸ ¾Æ´Ï¶ó º¸´Ù °ß°íÇÑ ÀÓ»ó ÆÄÀÌÇÁ¶óÀÎÀ» °¡´ÉÇÏ°Ô Çϰí, ºÐÀÚ ¼öÁØ¿¡¼­ Á¤ÀÇµÈ Á¾¾ç ¾ÆÇü¿¡ ¸Â´Â Â÷¼¼´ë DNA º¹±¸ ¾à¹°À» À§ÇÑ ¹«´ë¸¦ ¸¶·ÃÇϰí ÀÖ½À´Ï´Ù.

¾Ï ÀÌ¿ÜÀÇ Ä¡·á ¿µ¿ª È®´ë·Î ½ÃÀå °¡´É¼º È®´ë?

DNA º¹±¸ ¾à¹°ÀÇ ÁÖ¿ä ¿ëµµ´Â ¿©ÀüÈ÷ ¾Ï Ä¡·áÀÌÁö¸¸, ÀÌµé ¾à¹°ÀÇ ÀáÀçÀû Ä¡·á ¹üÀ§´Â ¾Ï ÀÌ¿ÜÀÇ ´Ù¾çÇÑ ÁúȯÀ¸·Î È®´ëµÇ°í ÀÖ¾î ½ÃÀåÀÇ ÀáÀç·ÂÀ» Å©°Ô È®ÀåÇϰí ÀÖ½À´Ï´Ù. DNA º¹±¸ ¸ÞÄ¿´ÏÁòÀº ³ëÈ­, ¿°Áõ, ½Å°æº¯¼º µî À¯Àüü ºÒ¾ÈÁ¤¼ºÀÌ Áúº´ÀÇ ¹ßº´°ú ÁøÇà¿¡ °ü¿©ÇÏ´Â ¿µ¿ª¿¡¼­ Áß¿äÇÑ ¿ªÇÒÀ» ÇÕ´Ï´Ù. ¾ËÃ÷ÇÏÀ̸Ӻ´, ÆÄŲ½¼º´, ÇåÆÃÅϺ´°ú °°Àº ½Å°æÅðÇ༺ Áúȯ¿¡¼­ DNA ¼Õ»ó ¹ÝÀÀ °æ·ÎÀÇ °áÇÔÀÌ ½Å°æ¼¼Æ÷ »ç¸ê°ú ÀÎÁö±â´É ÀúÇÏÀÇ ¿øÀÎÀ̶ó´Â Áõ°Å°¡ Á¡Á¡ ´õ ¸¹ÀÌ Á¦½ÃµÇ°í ÀÖ½À´Ï´Ù. ¿¬±¸ÁøÀº DNA º¹±¸ È¿¼Ò¸¦ Á¶ÀýÇÔÀ¸·Î½á Áúº´ÀÇ ÁøÇàÀ» ´ÊÃ߰ųª ½Å°æ º¸È£¸¦ °­È­ÇÒ ¼ö ÀÖ´ÂÁö ¿©ºÎ¸¦ Á¶»çÇϰí ÀÖ½À´Ï´Ù. ¸¶Âù°¡Áö·Î, ÀÚ°¡¸é¿ªÁúȯÀ̳ª ¿îµ¿½ÇÁ¶Áõ¼º ô¼öÈ®ÀåÁõ, ÆÇÄÚ´Ï ºóÇ÷°ú °°Àº Èñ±ÍÇÑ À¯Àü¼º Áúȯµµ DNA º¹±¸È¿¼Ò °áÇÌÀ¸·Î Ư¡Áö¾îÁö´Âµ¥, DNA º¹±¸È¿¼Ò¸¦ Á¶ÀýÇÏ´Â »õ·Î¿î Ä¡·á¹ýÀ¸·Î ÁÖ¸ñ¹Þ°í ÀÖ½À´Ï´Ù. ¶ÇÇÑ, ¹æ»ç¼± ³ëÃâÀº ¾Ï Ä¡·á·Î ÀÎÇÑ °ÍÀ̵ç ȯ°æÀûÀÎ °ÍÀ̵ç DNA ¼Õ»óÀ» À¯¹ßÇϱ⠶§¹®¿¡ DNA º¹±¸ ÃËÁøÁ¦¸¦ °³¹ßÇÔÀ¸·Î½á °Ç°­ÇÑ Á¶Á÷À» º¸È£Çϰí Àå±âÀûÀÎ ¿µÇâÀ» ¿ÏÈ­ÇÒ ¼ö ÀÖ½À´Ï´Ù. Á¦¾à»çµéÀº ¾Ï ¿µ¿ª¿¡¼­´Â ¾ïÁ¦Á¦·Î, ´Ù¸¥ Áúȯ¿¡¼­´Â º¸È£Á¦·Î, Àû¿ë ¹æ¹ý¿¡ µû¶ó ¾ç¸éÀ¸·Î »ç¿ëÇÒ ¼ö ÀÖ´Â ºÐÀÚ¸¦ ¸ð»öÇϰí ÀÖ½À´Ï´Ù. ÀÌ·¯ÇÑ Ä¡·áÀû À¯¿¬¼ºÀº DNA º¹±¸ ¾à¹° Èĺ¸¹°ÁúÀÇ »ó¾÷Àû ¸Å·ÂÀ» ³ôÀ̰í, ´õ ±¤¹üÀ§ÇÑ R&D ÅõÀÚ¸¦ ÃËÁøÇϰí ÀÖ½À´Ï´Ù. ƯÈ÷ °Ç°­ ¼ö¸íÀÇ ÇÙ½ÉÀÎ À¯Àüü À¯Áö¿¡ ÃÊÁ¡À» ¸ÂÃá ³ëÈ­ ¿¬±¸ÀÇ ºÎ»óÀº DNA º¹±¸ °æ·Î¸¦ ÀáÀçÀûÀÎ °³ÀÔ Æ÷ÀÎÆ®·Î ÁÖ¸ñÇϰí ÀÖ½À´Ï´Ù. °úÇа谡 DNA ¼Õ»ó, ¸¸¼ºÁúȯ, ¼¼Æ÷ ³ëÈ­ÀÇ »óÈ£ ¿¬°ü¼ºÀ» °è¼Ó ޱ¸ÇÏ´Â °¡¿îµ¥, DNA º¹±¸ ¾à¹°ÀÇ °ü·Ã¼ºÀº ¾ÏÀ» ³Ñ¾î ÈξÀ ´õ È®ÀåµÇ¾î °¡Ä¡ ÀÖ´Â ÀÓ»óÀû ÀÀ¿ëÀ» ½ÇÇöÇϰí ÀÖ½À´Ï´Ù.

DNA º¹±¸ ¾à¹° ½ÃÀåÀÇ ¼ºÀåÀ» ÃËÁøÇÏ´Â ¿äÀÎÀº ¹«¾ùÀΰ¡?

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Global DNA Repair Drugs Market to Reach US$19.5 Billion by 2030

The global market for DNA Repair Drugs estimated at US$8.3 Billion in the year 2024, is expected to reach US$19.5 Billion by 2030, growing at a CAGR of 15.2% over the analysis period 2024-2030. Targeted Therapy, one of the segments analyzed in the report, is expected to record a 17.2% CAGR and reach US$8.5 Billion by the end of the analysis period. Growth in the Hormonal Therapy segment is estimated at 11.8% CAGR over the analysis period.

The U.S. Market is Estimated at US$2.2 Billion While China is Forecast to Grow at 14.2% CAGR

The DNA Repair Drugs market in the U.S. is estimated at US$2.2 Billion in the year 2024. China, the world's second largest economy, is forecast to reach a projected market size of US$3.0 Billion by the year 2030 trailing a CAGR of 14.2% over the analysis period 2024-2030. Among the other noteworthy geographic markets are Japan and Canada, each forecast to grow at a CAGR of 14.3% and 12.9% respectively over the analysis period. Within Europe, Germany is forecast to grow at approximately 10.9% CAGR.

Global DNA Repair Drugs Market - Key Trends & Drivers Summarized

Is Targeting DNA Repair Mechanisms Redefining Cancer Therapy Paradigms?

The study of DNA repair mechanisms has revolutionized oncology by uncovering vulnerabilities in cancer cells that can be therapeutically exploited. DNA repair drugs, which target specific enzymes and pathways involved in maintaining genomic integrity, are at the forefront of this transformation. Cancer cells often rely heavily on alternative DNA repair mechanisms due to defects in their primary repair pathways-making them uniquely sensitive to targeted inhibition. This concept, known as synthetic lethality, is the foundation for several FDA-approved drugs, such as PARP (poly ADP-ribose polymerase) inhibitors, which have demonstrated remarkable efficacy in treating BRCA-mutated ovarian, breast, pancreatic, and prostate cancers. The promise of DNA repair inhibitors lies in their ability to selectively kill tumor cells while sparing normal cells, reducing off-target toxicity commonly associated with chemotherapy. Beyond PARP, the industry is actively exploring a range of targets including ATM, ATR, DNA-PK, CHK1/2, and POLQ, each playing vital roles in the cellular response to DNA damage. These emerging therapies are being evaluated as both monotherapies and combination regimens alongside immunotherapy, radiation, and traditional chemotherapy. The precision and personalization of DNA repair-targeted therapies are enabling more effective treatment strategies tailored to individual genomic profiles. Biomarker-driven drug development is thus central to this field, as companion diagnostics are used to identify patients most likely to benefit. As understanding of the DNA damage response (DDR) network deepens, DNA repair drugs are redefining the way cancers are treated-shifting from a one-size-fits-all model to a highly targeted, mechanism-specific approach that marks a new era in oncology.

How Are Advances in Genomics and Biomarker Science Powering Drug Development?

Technological advancements in genomics, sequencing, and molecular diagnostics are driving the development and clinical application of DNA repair drugs by enabling precise identification of DNA repair deficiencies in tumors. High-throughput sequencing and next-generation sequencing (NGS) platforms are now widely used to detect mutations in genes like BRCA1/2, ATM, PALB2, and other components of the homologous recombination repair (HRR) and mismatch repair (MMR) pathways. These insights allow clinicians and researchers to stratify patients based on their genetic makeup and predict treatment response more accurately. Furthermore, the discovery of novel genomic signatures such as "BRCAness" or homologous recombination deficiency (HRD) scores is expanding the eligibility criteria for DNA repair drugs beyond just germline BRCA mutations. Liquid biopsies, which detect circulating tumor DNA (ctDNA), are also gaining traction as minimally invasive tools to monitor treatment response and resistance in real time. Biomarker-guided drug development has become a key strategy for pharmaceutical companies, helping them design smarter clinical trials with enriched patient populations and higher success probabilities. Moreover, CRISPR-Cas9 gene editing is being used in preclinical models to better understand the role of specific DNA repair genes and their contribution to cancer progression, paving the way for the identification of new therapeutic targets. In silico modeling and AI-driven drug discovery platforms are also accelerating the identification of small-molecule inhibitors with higher selectivity and potency. These technological synergies are not only refining drug design but also enabling more robust clinical pipelines, setting the stage for a new generation of DNA repair drugs tailored to molecularly defined tumor subtypes.

Is the Expanding Therapeutic Scope Beyond Cancer Broadening Market Potential?

While oncology remains the primary application for DNA repair drugs, the potential therapeutic scope of these agents is expanding to include a variety of non-oncological conditions, which is significantly broadening the market’s potential. DNA repair mechanisms play a crucial role in aging, inflammation, and neurodegeneration-areas where genomic instability contributes to disease onset and progression. In neurodegenerative disorders like Alzheimer’s, Parkinson’s, and Huntington’s disease, growing evidence suggests that defects in DNA damage response pathways may contribute to neuronal death and cognitive decline. Researchers are investigating whether modulating DNA repair enzymes could slow disease progression or enhance neuroprotection. Similarly, autoimmune diseases and rare genetic disorders such as ataxia-telangiectasia and Fanconi anemia-characterized by inherent DNA repair deficiencies-are emerging as new therapeutic frontiers for DNA repair modulation. Moreover, radiation exposure, whether from cancer therapy or environmental sources, induces DNA damage, and DNA repair enhancers could be developed to protect healthy tissues or mitigate long-term effects. Pharmaceutical companies are exploring dual-use molecules that serve both as inhibitors in oncology and as protectants in other diseases, depending on how they are applied. This therapeutic flexibility increases the commercial attractiveness of DNA repair drug candidates, encouraging broader R&D investment. The rise of aging research, particularly focused on genome maintenance as a pillar of healthy longevity, is drawing attention to DNA repair pathways as potential intervention points. As the scientific community continues to explore the interconnectedness of DNA damage, chronic disease, and cellular aging, the relevance of DNA repair drugs is expanding far beyond cancer, unlocking a multitude of high-value clinical applications.

What Are the Core Drivers Fueling Growth in the DNA Repair Drugs Market?

The growth in the DNA repair drugs market is driven by several factors deeply rooted in scientific innovation, precision medicine, and evolving therapeutic strategies. A major driver is the growing prevalence of cancer worldwide, which is increasing demand for more targeted and less toxic therapies. DNA repair inhibitors, particularly PARP inhibitors, have already shown success in improving survival outcomes in BRCA-mutated and homologous recombination-deficient tumors, leading to rising adoption and new indications. The push toward personalized medicine is another key factor-clinicians are increasingly using molecular profiling to identify patients with DNA repair gene mutations who can benefit from these therapies. Advances in sequencing technologies and companion diagnostics are making such precision targeting more feasible and cost-effective. Additionally, the pharmaceutical industry’s expanding focus on combination therapies is playing a critical role in market growth, with DNA repair drugs being used alongside immune checkpoint inhibitors, chemotherapy, and radiation to enhance efficacy and overcome resistance. The increasing number of clinical trials exploring inhibitors of ATR, ATM, DNA-PK, and other DDR targets reflects a robust and growing development pipeline. Moreover, strategic collaborations between biotech startups and large pharmaceutical companies are accelerating the translation of early-stage research into viable therapeutic candidates. Regulatory bodies are also supporting innovation through fast-track designations, breakthrough therapy approvals, and expanded label indications for approved drugs. The emergence of real-world evidence from post-marketing studies is helping validate the long-term benefits of these treatments and guiding reimbursement decisions. Finally, public and private investments in oncology and aging research are creating a fertile environment for continued exploration of DNA repair biology, further propelling market momentum. These interconnected drivers are collectively positioning DNA repair drugs as a cornerstone of next-generation therapeutic strategies across oncology and beyond.

SCOPE OF STUDY:

The report analyzes the DNA Repair Drugs market in terms of units by the following Segments, and Geographic Regions/Countries:

Segments:

Breast Cancer Drugs Therapy (Targeted Therapy, Hormonal Therapy, Chemotherapy Therapy, Immunotherapy Therapy); Breast Cancer Drugs Cancer Type (Hormone Receptor Type, HER2+ Type); Breast Cancer Drugs Distribution Channel (Hospital Pharmacies, Retail Pharmacies, Other Distribution Channels)

Geographic Regions/Countries:

World; United States; Canada; Japan; China; Europe (France; Germany; Italy; United Kingdom; and Rest of Europe); Asia-Pacific; Rest of World.

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TABLE OF CONTENTS

I. METHODOLOGY

II. EXECUTIVE SUMMARY

III. MARKET ANALYSIS

IV. COMPETITION

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