Novel Solid Tumor Cancer Portfolio
Minerva Biotechnologies is developing cancer immunotherapies and cancer drugs to target 80% of solid tumors and to prevent cancer metastasis. We discovered that cancer cells are healthy cells that are being reprogrammed back to a stem cell state. We can reverse the reprogramming and make cancer cells mature so that cancer growth is turned off and cancer cell death pathways are turned on. This is a novel approach to curing cancer.
We have 3 anti-cancer therapeutics in our pipeline.
The single chain fragment variable (scFv) from our anti-MUC1* antibody is the targeting head for anti-MUC1* CARs (chimeric antigen receptor) for T cell immunotherapy. We have also developed proprietary CAR constructs with clean IP. Together this gives us complete CAR T therapeutics.
Our CAR T therapeutics will attack solid tumors that are MUC1* positive. This represents approximately 80% of all cancers, including 96-98% of breast cancers and very high percentages of patients with ovarian and pancreatic cancers and melanomas. The success of other CAR T companies has been limited to blood cancers.
Minerva is aiming to be in clinical trials in 2017 with an initial focus on patients with advanced breast and ovarian cancers.
Antibody Therapeutic for MUC1* Positive Cancers
We have humanized anti-MUC1* antibodies. We have developed a humanized high affinity, high specificity antibody fragment (scFv) that binds to MUC1* as it exists on cancer cells.
An anti-MUC1* fragment has been shown to block androgen-insensitive prostate cancer and breast cancer growth in vitro and in animals, without any detectable off-target effects. Our studies show that even though MUC1 is cleaved to a truncated form on some healthy cells, such as on hematopoietic stem cells in the bone marrow (to form all blood cells), our lead monoclonal antibody does not bind to them. Animal studies confirmed that the anti-MUC1* fragment had no adverse effect on their bone marrow cells.
Minerva has also discovered a metastatic growth factor. This ‘Met Factor’ should not be expressed in adults except in testis. However, we have found it in every metastatic cancer we have looked at.
Human cancer cells grown in this recombinant human Met Factor are able to form tumors in mice from the implantation of as few as 50 cancer cells. This indicates that they are metastatic since tumor formation in an animal usually requires 4-6 million human cancer cells.
Injecting Met Factor into these mice made these human cancers metastasize to the same organs and bone as human cancer would metastasize. This has never been done before.
We are developing an antibody therapeutic against this testis specific cancer antigen. Minerva has developed specific antibodies that block this growth factor and block the transition from a regular cancer cell to a metastatic cancer cell. Un-optimized anti-Met factor antibodies block cancer growth. Our optimized antibodies specifically block Met Factor but not related family members that are expressed in adults.
We made novel anti-‘Met Factor’ antibodies that block interaction of ‘Met Factor’ with its cognate receptor. We also identified ‘Met Factor’ peptides that inhibit interaction of ‘Met Factor’ with MUC1* – these could be used for vaccine.
MUC1* is not MUC 1
For more than 26 years the transmembrane protein MUC1 was known to exist in a different pattern on cancer cells than on healthy cells. However, scientists couldn’t figure out if its aberrant pattern was an artifact of cancer or a cause of cancer.
Minerva discovered that on cancer cells, MUC1 is cleaved and most of the protein is released from the cell surface, unmasking the binding site for a powerful growth factor. The cleavage released a part of the protein that kept it in a clustered pattern; clustering also masked the binding site for the activating growth factor. Minerva gave the cleaved MUC1 the name MUC1* (pronounced muk 1 star).
Minerva has discovered that MUC1* is a powerful growth factor receptor that mediates the growth of over 80% of all solid tumor cancers. Minerva has identified that it plays a foundational role in the both the rapid growth of cancer cells and their acquired chemo-resistance to common therapeutics. The Company has shown that inhibiting the MUC1* receptor can block cancer cell growth and also reverse acquired resistance to anti-cancer drugs, including Herceptin.
Prior attempts to produce a cancer therapeutic targeting MUC1 all failed as they targeted the extra cellular component of MUC1 that has been clipped and is no longer present on cancerous cells.