Candel Therapeutics Inc (NASDAQ:CADL) announced that preclinical data from its CAN-3110 program indicate promising antitumor activity in melanoma, suggesting a potential expansion beyond the candidate’s original focus on recurrent high-grade glioma.
The findings, to be presented at the Society for Immunotherapy of Cancer (SITC) annual meeting, highlight CAN-3110's dual mechanisms of oncolysis and immune activation in melanoma models.
CAN-3110, an oncolytic viral immunotherapy derived from herpes simplex virus-1, is designed to target cancer through both tumor destruction and immune activation.
Designed to target Nestin-expressing cancer cells, CAN-3110’s activity is specifically conditional upon the presence of this protein, which is expressed in certain solid tumors, including high-grade glioma and melanoma.
Candel CEO Paul Peter Tak told investors that the “encouraging” preclinical data helps to validate the broader potential of CAN-3110 in treating Nestin-positive solid tumors.
“The data supports the ability of CAN-3110 to selectively target and kill Nestin-positive tumor cells while eliciting profound immune activation,” Tak said in a statement.
The preclinical results demonstrated CAN-3110's potent antitumor activity both in vitro and in murine melanoma models, exhibiting dose-dependent tumor inhibition and tumor regression in certain cases. The treatment led to systemic immune activation, including a marked increase in circulating T cells, which mirrors responses observed in high-grade glioma.
“We are excited by the possibility to develop a new pipeline in a product centered around this first-in-class experimental medicine”.
Melanoma shares genetic traits with high-grade glioma, particularly high levels of Nestin and alterations in the CDKN2A tumor suppressor gene, Candel chief scientific officer Dr Francesca Barone explained.
"These similarities position CAN-3110 as a promising viral immunotherapy candidate for melanoma,” Barone added.
Candel’s new data will be presented at the SITC meeting in Houston from November 6 to 10.