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2025-05-13 07:00 Kvartalsrapport 2025-Q1
2025-02-21 07:00 Bokslutskommuniké 2024
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2023-05-24 - X-dag ordinarie utdelning CANTA 0.00 SEK
2023-05-23 - Årsstämma
2023-05-23 - Kvartalsrapport 2023-Q1
2023-02-23 - Bokslutskommuniké 2022
2022-11-10 - Kvartalsrapport 2022-Q3
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2022-07-21 - Extra Bolagsstämma 2022
2022-05-24 - X-dag ordinarie utdelning CANTA 0.00 SEK
2022-05-23 - Årsstämma
2022-05-23 - Kvartalsrapport 2022-Q1
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2021-08-19 - Kvartalsrapport 2021-Q2
2021-05-27 - X-dag ordinarie utdelning CANTA 0.00 SEK
2021-05-26 - Årsstämma
2021-05-26 - Kvartalsrapport 2021-Q1
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2020-05-28 - X-dag ordinarie utdelning CANTA 0.00 SEK
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2019-05-28 - X-dag ordinarie utdelning CANTA 0.00 SEK
2019-05-27 - Årsstämma
2019-05-27 - Kvartalsrapport 2019-Q1
2019-02-27 - Bokslutskommuniké 2018
2018-11-15 - Kvartalsrapport 2018-Q3
2018-08-21 - Kvartalsrapport 2018-Q2
2018-06-01 - X-dag ordinarie utdelning CANTA 0.00 SEK
2018-05-31 - Årsstämma
2018-05-15 - Kvartalsrapport 2018-Q1
2018-02-28 - Bokslutskommuniké 2017
2017-11-15 - Kvartalsrapport 2017-Q3
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2017-05-31 - X-dag ordinarie utdelning CANTA 0.00 SEK
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2016-03-01 - Bokslutskommuniké 2015
2015-11-17 - Kvartalsrapport 2015-Q3
2015-08-25 - Kvartalsrapport 2015-Q2
2015-05-19 - Kvartalsrapport 2015-Q1
2015-03-03 - Bokslutskommuniké 2014

Beskrivning

LandSverige
ListaSmall Cap Stockholm
SektorHälsovård
IndustriBioteknik
Cantargia är ett läkemedelsbolag. Idag återfinns specialisering mot utveckling av antikroppsläkemedel som används vid behandling av leukemi samt övriga cancersjukdomar som lung- och pankreascancer. Bolagets målsättning är att utveckla, sälja och licensiera läkemedelskandidater till bolag verksamma inom arbetsområdet. Störst verksamhet återfinns inom den nordiska marknaden, med huvudkontoret i Lund.
2024-04-17 17:00:00

Cantargia (Cantargia AB; Nasdaq Stockholm: CANTA) today reported publication of new preclinical data in the highly reputable scientific journal Cell Reports on the clinical stage antibody CAN10, specifying the precise interactions between CAN10 and its target IL1RAP and highlighting its functional capabilities to block multiple signaling pathways. These analyses explain the unique properties that makes CAN10 a potent blocker of the disease-promoting inflammatory cytokines IL-1, IL-33 and IL-36. This mechanism could be of high value in the treatment of a large number of diseases.

“The new results are important for our detailed understanding of the clinical stage CAN10 antibody, while also bringing light on the opportunity to affect multiple signaling pathways by targeting a single common receptor. This publication highlights the Cantargia antibodies and clearly verifies the external interest in this biological segment” said Göran Forsberg, CEO of Cantargia.

CAN10 is an IL1RAP-binding antibody in Phase I clinical development for treatment of autoimmune and inflammatory diseases. It has unique properties as it simultaneously blocks three inflammatory pathways important in several diseases. The data, now published in the journal Cell Reports, show in detail how CAN10, by binding to a specific part of IL1RAP, can efficiently block the IL-1 α/β, IL-33, and IL-36 α/β/γ signaling pathways. The publication also details biophysical and structural properties of the interaction between CAN10 and IL1RAP and shows that IL1RAP blockade has functional impact in counteracting inflammation beyond blocking only the IL-1 signaling pathway.

In addition, the now published data also details the binding and function of a second Cantargia anti-IL1RAP antibody, 3G5, which also efficiently blocks IL-1 a/b, IL-33, and IL-36 a/b/g signaling but does this via a molecular mechanism distinct from the one employed by CAN10. Thus, the new results combined with the knowledge in the Cantargia IL1RAP innovation platform add sophisticated understanding to the structure/function properties of targeting IL1RAP and thereby allows for continued strategic development of new therapeutic antibodies, tailored for specific medical needs.

The article, titled “Antibodies targeting the shared cytokine receptor IL-1 Receptor Accessory Protein (IL-1RAcP) invoke distinct mechanisms to block signaling by IL-1RAcP dependent cytokines”, was generated in a collaboration with the group of Prof. Eric J Sundberg at Emory School of Medicine, Atlanta, Dr. James Fields at Johns Hopkins School of Medicine, Baltimore, and Prof. Thoas Fioretos at Lund University. The article is available via the following link: https://www.cell.com/cell-reports/fulltext/S2211-1247(24)00427-3.