DNAtrix Announces Preclinical Data Demonstrating Anti-Tumor Activity of DNX-2401 in Models of Pediatric Tumors (AT/RT and CNS-PNET) Published in Clinical Cancer Research
HOUSTON, TX, February 11, 2021 -- DNAtrix, a biotech company advancing virus-driven immunotherapies for cancer, today announced preclinical data evaluating the use of DNX-2401 against the pediatric brain malignancies atypical teratoid/rhabdoid tumor (AT/RT) and primitive neuroectodermal tumors (PNETs) was published in Clinical Cancer Research. The data demonstrate that the oncolytic immunotherapy, DNX-2401 (tasadenoturev; Delta-24-RGD), induces a potent anti-tumor immune response, hinders the development of disseminated disease, and leads to longer survival in these difficult-to-treat tumors.
“These preclinical data for DNX-2401 show encouraging signals of anti-tumor activity against devastating CNS cancers that we had not previously studied,” said Jeffrey Knapp, chief executive officer of DNAtrix. “We now have preclinical and clinical data of DNX-2401’s efficacy across a range of difficult-to-treat adult and pediatric tumors, thus further establishing the activity of this potent immunotherapy. We look forward to the continued advancement of DNX-2401, as well as our pipeline of other oncolytic immunotherapies being developed for the treatment of solid tumors.”
The administration of DNX-2401 resulted in extended overall survival in early and advanced PNET and AT/RT mouse models, including models of disseminated disease. Importantly, DNX-2401 also generated a proinflammatory environment at tumor sites by boosting anti-tumor immune responses and inducing the secretion of damage-associated molecular patterns (DAMPs) into the extracellular medium by infected tumor cells.
Marta Alonso, Ph.D., associate professor at the Clinic University of Navarra-CIMA in Pamplona, Spain, added, “AT/RTs and CNS-PNETs are aggressive pediatric brain tumors that are associated with poor survival and have few therapeutic options. Based on promising clinical data of DNX-2401 in adult glioblastoma and pediatric diffuse intrinsic pontine glioma (DIPG), we evaluated its activity in AT/RT and CNS-PNET. These preclinical data demonstrate in vivo efficacy of DNX-2401 in established models that recapitulate important features of these tumors, including models for disseminated AT/RT lesions and in immunocompetent humanized mice. These data underscore the therapeutic potential of DNX-2401 and provide a strong foundation for translation to the clinical setting for these indications.”
DNX-2401 is an oncolytic adenovirus engineered specifically to infect, replicate in, and directly kill cancer cells, as well as elicit a broader anti-tumor immune response. DNX-2401 is currently being evaluated as a potential treatment for highly aggressive brain tumors, including recurrent glioblastoma in adults and newly-diagnosed diffuse intrinsic pontine glioma (DIPG) in children. Clinical studies have demonstrated that DNX-2401 was well tolerated and extended survival for patients with recurrent glioblastoma. DNX-2401 has been granted Fast Track and Orphan designation by the FDA and PRIME and Orphan designation by the EMA.
DNAtrix is a privately held biotech company developing virus-driven immunotherapies to treat cancer. Its proprietary adenovirus platform is based on an engineered version of the common cold virus that is designed to selectively infect and kill cancer cells while leaving healthy cells unharmed. The company’s lead product candidate is DNX-2401, which will enter into a global pivotal Phase 3 clinical study for patients with recurrent glioblastoma. DNX-2401 is also being evaluated in a Phase 1 study for diffuse intrinsic pontine glioma, for which it has received FDA Fast Track and Rare Pediatric Disease designations. A second product candidate, DNX-2440, is in Phase 1 clinical testing in patients with colorectal and other cancers with liver metastasis. The company’s investors include Morningside Ventures and Mercury Fund. For more information, please visit the company website at www.DNAtrix.com.
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