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Cantargia publishes an abstract on parallel anti-tumor activity and reduction of chemotherapy-induced neuropathy with nadunolimab
Prenumeration
Beskrivning
| Land | Sverige |
|---|---|
| Lista | Small Cap Stockholm |
| Sektor | Hälsovård |
| Industri | Bioteknik |
- Nadunolimab’s additional potential in mitigating neuropathy demonstrated by data from Cantargia’s CESTAFOUR and CAPAFOUR clinical studies
- Potential neuroprotective effect further supported in preclinical models
Cantargia (Cantargia AB; Nasdaq Stockholm: CANTA) today announced the publication of an abstract on the American Association for Cancer Research (AACR) website highlighting the potential neuroprotective role of nadunolimab (CAN04) in addition to its reported anti-tumor benefits. The anti-tumor efficacy of nadunolimab in metastatic pancreatic cancer (PDAC) is strongly supported by the outcomes observed in the CANFOUR Phase 2 study (NCT03267316), where the 60% of patients that had high IL1RAP expression showed a 48% ORR and 14.2 months OS. Beyond tumor control, higher nadunolimab doses were associated with both a lower incidence and a delayed onset of chemotherapy-induced peripheral neuropathy (CIPN). This neuroprotective activity is now supported by data from two additional clinical studies. These findings strongly suggest that nadunolimab offers neuroprotective benefits in addition to therapeutic efficacy.
“We’re very encouraged by this potential additional benefit of nadunolimab in reducing the severity and occurrence of CIPN on top of its promising survival benefit. CIPN results in an additional burden for the patient to deal with, impacts their ability to continue treatment and often has a long-lasting negative effect on the patient’s quality of life. We very much look forward to future studies to confirm this dual benefit of nadunolimab, particularly for the treatment of PDAC.” said Dominique Tersago, Chief Medical Officer, Cantargia.
Standard-of-care cancer treatments such as chemotherapy and antibody-drug conjugates (ADCs) can trigger inflammatory signals that promote peripheral neuropathy, a major and limiting side effect of these treatments. CIPN both limits treatment and severely impacts quality of life for patients. Based on the clinical findings in CANFOUR, nadunolimab’s potential in counteracting neuropathy associated with chemotherapy was further investigated.
Nadunolimab’s potential to mitigate FOLFOX-induced CIPN was assessed among 14 patients across eight cancer types in the CESTAFOUR (NCT05116891) study. Patients treated with 1 mg/kg of nadunolimab experienced a significantly delayed onset (p=0.0004) and a lower incidence (43% vs. 100%) compared to the 0.5 mg/kg dose group. Similar trends of CIPN onset and incidence were observed in the CAPAFOUR (NCT04990037) study, where 18 PDAC patients received FOLFIRINOX in combination with escalating doses of nadunolimab (0.5–2.5 mg/kg).
Complementary preclinical studies showed that combining a nadunolimab surrogate antibody with various chemotherapy drugs completely inhibited CIPN in mouse models, highlighting IL1RAP-driven neuroinflammation as a potential underlying mechanism driving CIPN.
The preclinical data were generated in collaboration with Dr. Hana Starobova and colleagues University of Queensland, Australia. The abstract title and texts will be posted onto the AACR online itinerary planner for the upcoming annual meeting in Chicago, IL on Apr 25-30, 2025, which can be accessed through the conference website https://www.aacr.org./