{"id":49,"date":"2018-12-20T00:11:47","date_gmt":"2018-12-20T04:11:47","guid":{"rendered":"https:\/\/www.creativebiomart.net\/alzheimacy\/?page_id=49"},"modified":"2020-09-06T23:53:27","modified_gmt":"2020-09-07T03:53:27","slug":"therapeutic-antibody","status":"publish","type":"page","link":"https:\/\/www.creativebiomart.net\/alzheimacy\/therapeutics\/therapeutic-antibody\/","title":{"rendered":"Therapeutic Antibody"},"content":{"rendered":"\n<p><strong>Using Therapeutic Antibodies Against Alzheimer&rsquo;s Disease<\/strong><\/p>\n<p>\n        The most interesting results obtained in  animal models of  passive immunotherapies developed according to the &ldquo;amyloid-beta cascade  hypothesis&rdquo; and the &ldquo;Tau hypothesis&rdquo; are monoclonal antibodies that directly or  indirectly target A\u03b2 plaques or neurofibrillary  tangles. Unfortunately, these therapeutic antibodies cannot replicate their  promising effects on  humans at the clinical phase. Despite this, we still hope to learn from these  failures and to  explore new pathways. The great effects obtained in animals with passive  immunotherapy suggest that this technology may be an important key to curative treatment. The  remaining challenge is to find a way to achieve the same encouraging results for humans. Alzheimacy expects to join hands with global  partners to focus on the development of therapeutic antibodies for Alzheimer&rsquo;s disease  (AD) and continue to fight against this disease. <\/p>\n<p class=\"ServiceShowPic\"><img decoding=\"async\" width=\"800\"  src=\"https:\/\/www.creativebiomart.net\/alzheimacy\/wp-content\/themes\/alzheimacy\/images\/Therapeutic-Antibody-1.jpg\"><\/p>\n<p><strong>Several  Pending Issues to Increase Efficacy of Passive Immunotherapies<\/strong><\/p>\n<ul>\n<li><strong>Increasing  brain uptake of antibodies<\/strong>: Because of the presence of  blood-brain barrier that prevents macromolecules from entering the brain, only a  small fraction of injected antibodies can reach the brain. Recombinant antibody  production methods have led to the production of novel antibody formats, such  as bispecific antibodies and antibody drug conjugates, which have the ability  to overcome low blood-brain barrier permeability. In addition, it is also a  strategy to use the gene therapy vectors to trigger the expression of  therapeutic antibodies in the brain.<\/li>\n<li><strong>Prevention  of side effects<\/strong>: Some clinical trials of therapeutic antibodies  have been  discontinued due to severe side effects, such as vasogenic edema and  microhemorrhages caused by the activation of the antibody&rsquo;s effector function.  One method of preventing the occurrence of side effects could be a slower and  more gradual increase in dose administration.<\/li>\n<li><strong>Exploring  new pathways<\/strong>: Previous clinical failures of  therapeutic antibodies targeting A\u03b2 plaques have forced researchers to consider  exploring new pathways. Therefore, more and more Tau fibril-targeted antibodies  are reaching the early clinical phases.  In addition, we should be more active in finding better therapeutic targets,  and in this process, we should be cautious about the absolute effectiveness of  AD transgenic animal models.<\/li>\n<\/ul>\n<p><strong>About  Alzheimacy<\/strong><\/p>\n<p>\n        Alzheimacy is dedicated to transforming  knowledge about the underlying mechanisms of AD into effective therapeutics. We  are willing to collaborate with leaders and scientists from academia, pharmaceutical and  biotechnology companies around the world to develop therapeutic antibodies  for this disease.<\/p>\n<ul>\n<li><strong>Basic  Research<\/strong><\/li>\n<\/ul>\n<p>Some neuropathologic features of AD have  been well characterized, but it is still unclear what mechanism is  responsible for the occurrence and development of the disease. A\u03b2 plaques, neurofibrillary tangles, as  well as cholinergic neuron damages, oxidative stress and inflammatory reactions  in AD patients, all of these  pathological expressions are  obviously linked to each other. However, determining the origins of &ldquo;chicken&rdquo; and  &ldquo;egg&rdquo; on a global scale is rather sophisticated, making the development of  effective and radical therapies particularly difficult. Despite this, we still  hope to help people better understand the disease and advance basic research to the early diagnosis and treatment  of the disease by leveraging our comprehensive and powerful technology  platform. The accumulation of long-term  experience in  the fields of biology, chemistry and crossover fields of life sciences (such as  computer science) gives us the strength to study the pathogenesis of the  disease in depth.<\/p>\n<ul>\n<li><strong>Pre-clinical  Development<\/strong><\/li>\n<\/ul>\n<p>As a leader in  the field of life science, Alzheimacy has established an integrated antibody  discovery and engineering platform. Our comprehensive antibody development  capabilities include but are not limited to target discovery and validation,  surface display technologies and antibody library screening, antibody  humanization and affinity maturation, pilot production of therapeutic  antibodies, efficacy study and safety evaluation of therapeutic antibodies.<\/p>\n<p>\n        In the process  of antibody discovery, our hybridoma, phage display, B cell sorting, and other  technologies give us strong support. Our transgenic design and technology allow  for potent antibody gene rearrangement, class switching, and somatic  hypermutation, which is the foundation for yielding diversified antibody pools. Moreover, we support the development of antibodies at the extra small size that allows for increased flexibility, better penetration (<em>i.e<\/em>. cross the blood-brain barrier), higher conformational epitope accessibility, and easier production. Long-term experience in the creation and assessment of animal  models supports our preclinical assessment for AD therapeutic antibodies.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Using Therapeutic Antibodies Against Alzheimer&rsquo;s Disease The most interesting results obtained in animal models of passive immunotherapies developed according to the &ldquo;amyloid-beta cascade hypothesis&rdquo; and the &ldquo;Tau hypothesis&rdquo; are monoclonal antibodies that directly or indirectly target A\u03b2 plaques or neurofibrillary tangles. Unfortunately, these therapeutic antibodies cannot replicate their promising effects on humans at the clinical [&hellip;]<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":11,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":[],"_links":{"self":[{"href":"https:\/\/www.creativebiomart.net\/alzheimacy\/wp-json\/wp\/v2\/pages\/49"}],"collection":[{"href":"https:\/\/www.creativebiomart.net\/alzheimacy\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/www.creativebiomart.net\/alzheimacy\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/www.creativebiomart.net\/alzheimacy\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/www.creativebiomart.net\/alzheimacy\/wp-json\/wp\/v2\/comments?post=49"}],"version-history":[{"count":5,"href":"https:\/\/www.creativebiomart.net\/alzheimacy\/wp-json\/wp\/v2\/pages\/49\/revisions"}],"predecessor-version":[{"id":80,"href":"https:\/\/www.creativebiomart.net\/alzheimacy\/wp-json\/wp\/v2\/pages\/49\/revisions\/80"}],"up":[{"embeddable":true,"href":"https:\/\/www.creativebiomart.net\/alzheimacy\/wp-json\/wp\/v2\/pages\/11"}],"wp:attachment":[{"href":"https:\/\/www.creativebiomart.net\/alzheimacy\/wp-json\/wp\/v2\/media?parent=49"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}