Developing Hapentized
Haptenization is based on proven science, a well-understood mechanism of action, and extensive clinical data, with evidence that it can be used to treat multiple viral infections and any resectable solid tumor.
Inducing Targeted T-Cell
and Antibody Response
The BioVaxys vaccine platform is based on the concept of haptenization. This idea has a long history, beginning with the work of the immunologist and Nobel laureate Dr. Karl Landsteiner,
Simply put, the process of haptenization “teaches” a patient’s immune system to recognize and make target proteins more ‘visible’ as foreign, thereby stimulating a more intense immune response. We now understand that T-cells (or T-lymphocytes, which are white blood cells that are crucial in tumor rejection) react against the haptenized material and that the T-cells also then react against the unmodified target protein. At BioVaxys, we believe that tumor and viral antigens, which are proteins, are similarly affected by haptenization which stimulates a T-cell mediated immune response.
Besides having no observed toxicity in multiple clinical trials, haptenization is based on proven science, a well-understood mechanism of action, and extensive clinical data, with evidence that it can be used to treat multiple viral infections and any resectable solid tumor.
SARS-CoV-2
Vaccine Development
BVX-0320:
Our lead IND-stage vaccine candidate for SARS-CoV-2.
In vivo studies have demonstrated that BVX-0320, BioVaxys’ monovalent haptenized s-spike protein vaccine, stimulated a 96.4% antibody response, activation of CD4+ helper T cells and CD8+ killer T cells, and stimulation of T cells that produce the cytokine, gamma interferon. Helper CD4+ T-cells are memory cells that retain information about the virus, enabling them to respond rapidly after viral exposure. CD8+ T cells have the capacity to kill cells infected by the virus, thereby stopping viral replication in those cells. Furthermore, our clinical experience with haptenization and safety data from prior clinical development of haptenized vaccines may prove advantageous from a regulatory perspective and lead to an accelerated development process.
BioVaxys is assessing steps to develop a multivalent version of BVX-0320 to address newly emerging SARS-CoV-2 variants such as the highly transmissible United Kingdom (B.1.1.7 lineage), South Africa (B.1.351 lineage), and Brazil (P.1 lineage) that are of high concern to worldwide governments, healthcare practitioners, and infectious disease researchers.
Bi-Haptenized Ovarian Cancer Tumor Cell Vaccine
BVX-0918A: Our lead haptenized tumor cell vaccine for ovarian cancer.
BioVaxys’s cancer vaccines are created by extracting a patient’s own (e.g. ‘autologous’) cancer cells, chemically treating them with a hapten, and re-injecting them into the patient to induce an immune response to proteins which are otherwise not immunogenic. Haptenization is a well-known and well-studied immunotherapeutic approach in cancer treatment, and has been clinically evaluated in both regional and disseminated metastatic tumors. A first generation single-hapten vaccine achieved positive immunological and clinical results in Phase I/II trials. At BioVaxys, we have enhanced this first generation approach to now utilize two haptens (“bi-haptenization”) which we believe will yield superior results.
Single haptenization only modifies hydrophilic amino acids on antigenic proteins, but utilizing two different haptens modifies both both hydrophilic and hydrophobic amino acids on these target proteins, making the protein more foreign to the immune system with modification of additional amino acids. A greater number of T cells is activated by the addition of another hapten (i.e., more modified amino acids) so the number of T cells potentially reactive to the unmodified protein increases.
Further, we plan to combine the use of our vaccine with anti-CTLA4 and anti-PDA checkpoint antibodies. The rationale is that these reagents on their own are powerful augmenters of cellular immune response; We believe our vaccine changes the tumor environment to make them more susceptible to checkpoint mAbs (induction of TILs & activation markers), and we expect a synergistic response from the combination.
