Our science
Harnessing integrin allostery to reverse malignancy
AVIPERO Bio has developed a unique platform technology based on allosteric modulation of integrins — a fundamentally different approach to treating cancer and degenerative diseases.
What are integrins?
Integrins: the gatekeepers of cell behaviour
Integrins are transmembrane receptors that mediate cell adhesion to the extracellular matrix and transduce signals that regulate cell survival, proliferation, and migration.
In cancer and degenerative disease, integrin signalling is dysregulated — driving the malignant behaviours that make these conditions so difficult to treat.
The dimmer switch analogy
A dimmer switch, not an on/off switch
Conventional drugs act like an on/off switch — blocking receptor function entirely. Our allosteric approach acts like a dimmer switch, modulating receptor activity to restore normal cell behaviour rather than eliminating it.
"We restore. We don't destroy."
Mechanism of action
How AVI001 works
Cilengitide and volociximab were ligand-competitive: they occupied the binding pocket to block adhesion outright, and both failed in clinical development. AVI001 does not compete for the ligand site.
AVI001 (JB1a) is a humanised monoclonal antibody that binds the hybrid domain of β1 integrin — a regulatory interface remote from the ligand-binding pocket. By engaging this allosteric site, AVI001 holds the receptor in its low-affinity resting conformation, preventing the conformational switch to the active high-affinity state.
This selectivity for the hybrid domain means AVI001 does not interfere with normal integrin-mediated adhesion in healthy tissue, reducing the risk of the on-target toxicities that contributed to the failure of earlier integrin-targeted agents.
Platform applications
One mechanism. Multiple indications.
Cancer
β1 integrin activation drives tumour cell migration, invasion, and resistance to therapy. AVI001 targets this pathway across multiple solid tumour types.
Degenerative diseases
Aberrant integrin signalling contributes to fibrosis and neurodegeneration. Our platform offers a novel approach to modulating these pathological processes.
Viral infections
Certain viruses exploit integrin-mediated entry pathways. Our platform offers a novel approach to blocking viral infection at the cell surface.
Our approach
Restoring cells, not destroying them
Our targeted therapeutic pharmacology refines integrins and tissues instead of killing them. This transformative nature of our platform comes from our unique understanding of changes in cell behaviour in different illnesses.
This approach retains rogue cells which cause malignant tumours. Instead of shutting them down, it brings them back to their original state, therefore modifying disease progression and reducing severe side effects.
This form of treatment has been proven effective on metastatic cancers as well as various degenerative diseases and viral infections.
Interested in our development programs?
Explore our pipeline of allosteric integrin modulators across multiple disease indications.
نبذة عربية
الأساس العلمي: التعديل الألوستيري للإنتيغرين
الإنتيغرينات مستقبلات عبر-غشائية على سطح الخلية تتحكم في التصاق الخلايا بالمصفوفة خارج الخلوية وتنقل الإشارات التي تنظّم بقاء الخلية وتكاثرها وهجرتها. في السرطان والأمراض التنكسية، يُصبح إشارات إنتيغرين بيتا-1 مضطربة، مما يُحرّك السلوكيات الخبيثة التي تجعل هذه الحالات بالغة الصعوبة في العلاج.
يختلف نهج أفيبيرو جذرياً عن الأدوية السابقة كـ Cilengitide وvolociximab التي اعتمدت على التنافس مع الروابط وأخفقت في التطوير السريري. يرتبط AVI001 بالنطاق الهجين لإنتيغرين بيتا-1 — واجهة تنظيمية بعيدة عن موقع ارتباط الرابط — ويُثبّت المستقبل في تشكّله منخفض الألفة في حالة الراحة دون أن يتنافس على موقع الرابط.
تمتد هذه المنصة عبر علم الأورام والأمراض التنكسية العصبية والعدوى الفيروسية، مما يُتيح فرصاً متنوعة للشراكات التطويرية الإقليمية، مدعومةً بأكثر من 15 عاماً من الأبحاث الموثّقة في جامعة إدنبرة.
中文简介
科学基础：整合素变构调节
整合素是细胞表面的跨膜受体，负责调控细胞与细胞外基质之间的黏附与信号传导。在癌症及多种退行性疾病中，β1整合素被异常激活，驱动肿瘤细胞的迁移、侵袭与存活。传统整合素药物（如Cilengitide和volociximab）采用配体竞争性抑制策略，直接封堵结合位点，但两者均在临床开发中失败。
Avipero的方法截然不同。AVI001（即JB1a）是一种人源化单克隆抗体，靶向β1整合素的混合结构域——一个远离配体结合位点的变构调节界面。通过将受体锁定在低亲和力静息构象，AVI001阻止整合素切换至激活状态，而无需竞争配体位点。这一机制赋予其独特的选择性，并在爱丁堡大学超过15年的研究中得到了充分的文献支持。
该平台的广度横跨肿瘤学、神经退行性疾病与病毒感染，为区域性开发合作提供了多元化的机会。