{"id":86235,"date":"2025-11-03T08:00:00","date_gmt":"2025-11-03T07:00:00","guid":{"rendered":"https:\/\/aktuelles.uni-frankfurt.de\/?p=86235"},"modified":"2025-11-01T10:03:02","modified_gmt":"2025-11-01T09:03:02","slug":"protacs-disposal-as-therapy","status":"publish","type":"post","link":"https:\/\/aktuelles.uni-frankfurt.de\/en\/english\/protacs-disposal-as-therapy\/","title":{"rendered":"PROTACs: \u201cDisposal\u201d as Therapy"},"content":{"rendered":"<p><strong>Pharmacist Manfred Schubert-Zsilavecz explains the new active substances.<\/strong><\/p>\n\n\n\n<p>Until now, almost all medications have influenced disease processes by either replacing missing molecules or blocking malfunctioning molecules (or their production). A new type of active substance, called \u201cProteolysis Targeting Chimera\u201d or PROTACs, takes a different approach: they use the cell\u2019s own \u201cwaste shredders\u201d to eliminate disruptive proteins. None of these substances have been approved yet, but a short while ago, an admissions application was submitted for Vebdegestrant (see below).<\/p>\n\n\n\n<div style=\"height:20px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<figure class=\"wp-block-image aligncenter size-full\"><img fetchpriority=\"high\" decoding=\"async\" width=\"650\" height=\"450\" src=\"https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2025\/10\/protac-c-andreas-kraemer.jpg\" alt=\"A PROTAC (green) acts like a \u201cmolecular glue,\u201d binding the disease-causing protein (blue) to the cellular recycling system (pink) and triggering its degradation. The illustration is based on a high-resolution protein structure characterized in Prof. Knapp\u2019s lab, which reveals the molecular details of the PROTAC-induced interaction. This structure was crucial in precisely optimizing the PROTAC glue. The resulting PROTAC molecule is currently being tested in preclinical cancer models, particularly for leukemia. Illustration: Andreas Kr\u00e4mer\" class=\"wp-image-86150\" srcset=\"https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2025\/10\/protac-c-andreas-kraemer.jpg 650w, https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2025\/10\/protac-c-andreas-kraemer-300x208.jpg 300w, https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2025\/10\/protac-c-andreas-kraemer-500x346.jpg 500w, https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2025\/10\/protac-c-andreas-kraemer-18x12.jpg 18w\" sizes=\"(max-width: 650px) 100vw, 650px\" \/><figcaption class=\"wp-element-caption\">A PROTAC (green) acts like a \u201cmolecular glue,\u201d binding the disease-causing protein (blue) to the cellular recycling system (pink) and triggering its degradation. The illustration is based on a high-resolution protein structure characterized in Prof. Knapp\u2019s lab, which reveals the molecular details of the PROTAC-induced interaction. This structure was crucial in precisely optimizing the PROTAC glue. The resulting PROTAC molecule is currently being tested in preclinical cancer models, particularly for leukemia. Illustration: Andreas Kr\u00e4mer<\/figcaption><\/figure>\n\n\n\n<div style=\"height:20px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<h2 class=\"wp-block-heading\">The Challenge<\/h2>\n\n\n\n<p>In many diseases, cells in the body produce far too much of a protein or produce it at the wrong time. Sometimes, harmful proteins are even produced that shouldn\u2019t exist at all. Treatments often involve medications that block either the relevant protein itself or its production.<\/p>\n\n\n\n<p>Two examples:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Many people produce too much cholesterol in their bodies. Statins are drugs that lower a key enzyme in the liver responsible for cholesterol biosynthesis, thereby reducing the body\u2019s cholesterol production.<\/li>\n\n\n\n<li>Headaches: Many headaches begin with the formation of certain pain substances by two enzymes called Cox1 and Cox2. Ibuprofen, aspirin, diclofenac, and naproxen block these enzymes, preventing pain from occurring.<\/li>\n<\/ul>\n\n\n\n<p>Over 20 years ago, scientists \u2013 including this year\u2019s endowed visiting professor \u2013 came up with a completely new idea: Every cell, they reasoned, has a protein shredder for waste. The question was: Could this shredder be directed to target the relevant enzyme or receptor, essentially breaking it down into tiny pieces? As it turns out, this is possible. The first drugs that work this way are currently being tested in clinical trials. They are called PROTACs, or \u201cProteolysis Targeting Chimeras.\u201d<\/p>\n\n\n\n<div style=\"height:20px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<h2 class=\"wp-block-heading\">How the shredder knows what to shred<\/h2>\n\n\n\n<p>The protein shredder in cells doesn\u2019t just break down everything it encounters. It only shreds a protein if a kind of cellular \u201clabeling machine\u201d has first attached a label saying \u201cready to go.\u201d The official name of this machine is Ligase E3. PROTACs need to bring the unwanted proteins together with this machine. To achieve this, researchers in pharmaceutical labs have developed compounds made of two parts: while one part is designed to bind to the \u201clabeling machine,\u201d the other is built to attach to the unwanted protein. When such medication is administered to a person, these dual molecules enter the cells and connect with the machine and the target protein. The machine labels the target protein, and the shredder takes care of the rest.<\/p>\n\n\n\n<div style=\"height:20px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<h2 class=\"wp-block-heading\">Diseases where PROTACs could help<\/h2>\n\n\n\n<p>Many companies are undertaking efforts to develop new treatment options for patients with a wide range of illnesses. For cancer alone, more than 70 different PROTACs are in development, targeting breast cancer, prostate cancer, lung cancer, lymphoma, and other types of the disease. But the focus isn\u2019t just on cancer \u2013 autoimmune diseases like rheumatoid arthritis or atopic dermatitis are also being addressed. These conditions require suppression of immune responses. While conventional medications already work well for many patients, they don\u2019t help everyone. In laboratories, researchers are experimenting to see if PROTACs could also be used to combat viruses, which \u2013 aided by viral proteins \u2013 invade cells and replicate within them. PROTACs could potentially ensure that these viral proteins are quickly eliminated. Another exciting field is neurodegenerative diseases, which often involve proteins that clump together and accumulate as waste in nerve cells. In Alzheimer\u2019s disease, these consist of aggregates of tau protein, which are also involved in frontotemporal dementia. In Parkinson\u2019s disease, alpha-synuclein aggregates play a role, while the same is true of aggregates of mutated huntingtin protein in Huntington\u2019s disease. There are currently no approved medications to prevent these protein aggregations. Some companies are now working to develop PROTACs to target these aggregates. If the aggregation itself can\u2019t be prevented, the goal is to shred the aggregates afterward. However, these PROTACs are still in the laboratory stage.<\/p>\n\n\n\n<div style=\"height:20px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<h2 class=\"wp-block-heading\">Admissions application for Vepdegestrant submitted to the FDA<\/h2>\n\n\n\n<p>On August 8, 2025, pharmaceutical companies Arvinas and Pfizer announced that they had submitted an admissions application to the FDA for the jointly developed protein degrader Vepdegestrant (1). This application is significant as it marks a milestone in the development of PROTACs, which have not been therapeutically available outside of clinical trials until now. PROTACs are orally administered bifunctional agents that induce the targeted degradation of disease-related proteins within cells. Vepdegestrant binds to the estrogen receptor (ER) with an estrogen-mimetic molecular component and to the E3 ligase with another molecular component. This induced proximity between the ER and E3 ligase leads to ubiquitinylation and, subsequently, the targeted degradation of the estrogen receptor protein by the cellular proteasome. Vepdegestrant is expected to be approved in 2026 for the treatment of patients with estrogen receptor-positive (ER+)\/human epidermal growth factor receptor 2-negative (HER2-) and ESR1-mutated breast cancer who have previously undergone endocrine therapy.<\/p>\n\n\n\n<div style=\"height:20px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p class=\"has-text-align-right\"><em>Prof. Dr. Manfred Schubert-Zsilavecz serves as Chair of the Board of Trustees for the Friedrich Merz Visiting Fellowship Endowment.<\/em><\/p>\n\n\n\n<div style=\"height:20px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p class=\"has-background\" style=\"background-color:#eeeeee\"><strong>PROTAC<\/strong><br>The name PROTAC stands for \u201cProteolysis Targeting Chimera.\u201d This agent is called a chimera because it consists of two completely different parts \u2013 similar to how the mythical chimera was composed of multiple animals. \u201cTargeting\u201d refers to aiming at something, while \u201cProteolysis\u201d is the scientific term for breaking down proteins. PROTACs, therefore, are chimeras designed to specifically target and break down proteins.<\/p>","protected":false},"excerpt":{"rendered":"<p>Pharmacist Manfred Schubert-Zsilavecz explains the new active substances. Until now, almost all medications have influenced disease processes by either replacing missing molecules or blocking malfunctioning molecules (or their production). A [&hellip;]<\/p>\n","protected":false},"author":8,"featured_media":86150,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_eb_attr":"","_price":"","_stock":"","_tribe_ticket_header":"","_tribe_default_ticket_provider":"","_ticket_start_date":"","_ticket_end_date":"","_tribe_ticket_show_description":"","_tribe_ticket_show_not_going":false,"_tribe_ticket_use_global_stock":"","_tribe_ticket_global_stock_level":"","_global_stock_mode":"","_global_stock_cap":"","_tribe_rsvp_for_event":"","_tribe_ticket_going_count":"","_tribe_ticket_not_going_count":"","_tribe_tickets_list":"[]","_tribe_ticket_has_attendee_info_fields":false,"footnotes":""},"categories":[126,254],"tags":[245,418],"post_folder":[],"class_list":["post-86235","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-english","category-research","tag-pharmacy","tag-unireport-5-25"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.4 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>PROTACs: \u201cDisposal\u201d as Therapy | Aktuelles aus der Goethe-Universit\u00e4t Frankfurt<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/aktuelles.uni-frankfurt.de\/en\/english\/protacs-disposal-as-therapy\/\" \/>\n<meta property=\"og:locale\" content=\"en_GB\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"PROTACs: \u201cDisposal\u201d as Therapy | Aktuelles aus der Goethe-Universit\u00e4t Frankfurt\" \/>\n<meta property=\"og:description\" content=\"Pharmacist Manfred Schubert-Zsilavecz explains the new active substances. 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Die Abbildung basiert auf einer hochaufgel\u00f6sten Proteinstruktur, die im Labor von Prof. Knapp charakterisiert wurde und die molekularen Details der durch PROTAC induzierten Interaktion sichtbar macht. Diese Struktur hat entscheidend dazu beigetragen, den PROTAC-Klebstoff pr\u00e4zise zu optimieren. Das darauf basierende PROTACMolek\u00fcl wird derzeit in pr\u00e4klinischen Krebsmodellen, insbesondere bei Leuk\u00e4mie, getestet. 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