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Our Solutions

Our next generation Mirror Effect® technology solves the key problems which inhibit the commercial expansion of first-generation immune checkpoint inhibitor and CAR-T cell immunotherapy technologies.

1. Checkpoint Inhibitor Problems

Checkpoint inhibition therapy only works in a subset of cancer patients that have highly mutated  “immunogenic” tumors, such as melanoma, non-small cell lung cancer and bladder cancer with the pre-requisite that the tumors lesions are infiltrated with resident killer immune cells that are pre-programmed to identify and kill the tumors but are suppressed by checkpoint molecules.  Only approximately 20% of immunogenic tumors have the requisite resident killer immune cells (“hot” tumors).  The majority of human tumors are “cold”, without educated killer cell infiltrates and are thus unable to respond to checkpoint blockade. 

Checkpoints are molecules expressed on most normal cells. When killer immune cells surveille normal cells, they encounter checkpoint molecules which send a “stand down” signal to the killer immune cells. This stand down signal prevents killer cells from killing normal cells. Checkpoint inhibition releases these stands down signals, permitting killer cells to kill tumors, but also normal cells. 

Tumor cells are transformed from normal cells and retain the expression of checkpoint molecules.  The expression of checkpoint molecules on tumor cells allows tumors to escape immune elimination. Checkpoint inhibitor drugs block checkpoint molecules, such as CTLA4 and PD-1/L1 interactions with immune cells, releasing the inhibition and enabling immune-mediated killing.

The systemic release of protective checkpoint molecule expression not only enables resident killer cells to kill tumors, but also permits the attack of normal cells. This results in significant autoimmune side effects that require special skills to recognize and manage. 

To increase the applicability and efficacy of checkpoint inhibitor drugs, many clinical trials are testing the combination of checkpoint inhibitors with each other and with other cancer treatments. These programs often increase efficacy at greater expense in terms of cost and toxicity  There are also efforts to combine checkpoint inhibitor drugs with therapeutic cancer vaccines in order to educate killer immune cells and convert “cold” tumors to “hot” tumors as a strategy to increase checkpoint applicability to broader tumor indications. 

Currently, the majority of patients treated with checkpoint inhibitor drugs experience the side-effects of the treatment without clinical benefit.

Ice Blocks
Image by Marc Renken

"Cold" to "Hot" tumor

Our Solution:

AlloStim® consistently causes non-immunogenic “cold” tumors to become “hot” with infiltration of activated innate killer cells and pre-programmed tumor-specific T-cells.  AlloStim® protocols modify the local tumor environment creating a high amount of inflammation.  The inflammatory microenvironment has the effect of naturally down-regulating checkpoint molecules in only the tumor lesions and surrounding cells and not on distant normal cells. Thus, AlloStim® can expand the indications responsive to immunotherapy without the autoimmune side-effects.

2. CAR-T Cell Therapy Problems

CAR-T cell immunotherapy involves the removal of a patient’s own T cells, placing these immune cells in culture outside the body, genetically engineering the cells to recognize a marker over-expressed on the surface of a tumor cell, expanding the genetically-altered immune cells in culture and then infusing the genetically altered cells back into the patient. There are several problems with this approach that inhibit the commercial viability and applicability.

The source material to manufacture the CAR-T drug are immune cells from the patient. Thus the drug is custom manufactured for each patient and the production can not be scaled-up. This removes any economy of scale and results in exorbitant product costs. The high price of manufacturing results in current CAR-T drug pricing from $375,000 to over $500,000.  Further, the poor condition of a heavily pre-treated cancer patient’s immune cells often results in failure to expand sufficient numbers of CAR-T cells for reinfusion, resulting in manufacturing expenses without any resulting product, further increasing operating costs. 

The reinfusion of CAR-T cells causes severe, life-threatening toxicity. This requires that CAR-T treatments be performed in a hospital or intensive care setting, which can increase the overall cost to over $1 million. However, the most major problem with commercial expansion of CAR-T cells is that this approach currently is only applicable to treating blood cancers.  

CAR-T cells are T-cells genetically engineered to recognize tumor cells like an antibody.


Cytolytic T-cells (CTL) (killer cells) are the most powerful anti-tumor immune cells.  CTL survellle all cells in the body for adnormalities though their T-cell receptor (TCR). The TCR on the CTL interacts with MHC I molecules expressed on cells.  If the cells has any mutated proteins or proteins from viruses, small segments of these mutated proteins are displayed on MHC I molecules,for recognition by the CTL through the TCR.  If a CTL recognizes the abnormal peptide and the transformed or infected cell expresses a co-stimulatory signal (mostly through CD28), the CTL killer program is engaged and the target cell will be lysed.  However, the identification of peptides that will be recognized by CTL is limited, making it difficult to program and direct CTL to specifically kill tumors.  The most advanced method to identify tumors is through the overexpression of surface molecules by antibodies.  However, antibodies are not able to kill tumors. Therefore, the concept behind CAR-T technology is to genetically modify CTL so that they recognize tumors like an antibody and kill like a CTL.

The major technical obstacle to CAR-T cells approach is the lack of surface molecules expressed only on tumors and not on normal cells in which to direct the CAR-T cells.  With abesence of tumor-specific markers, CAR-T can only be directed to tissue specific antigens. For example, antigens expressed on all B-cells.  Since in leukemia most all B-cells are tumor, by eliminating all B-cells, it has been shown that new heathly B-cells can later replace the killed leukemic cells. 

However, solid tumors are not tissue specific and thus CAR-T can not be genetically-engineered to attack solid tumors as they can for blood cancers.  This technical problem restricts use of CAR-T only to certain blood cancers where the targeted blood cell can be killed and replaced. 

Our Solution:

Mirror Effect® technology is able to harness the power of CTL to specifically kill tumors by reverse engineering natural immune mechanisms to educate and arm CTL to identify and kill solid tumor cells and not normal cells without need for genetic manipulation.  The process is enabled by “off-the-shelf” AlloStim® cells.  Thus, our next generation immunotherapy broadens the applicability of resident CTL tumor killing mechanisms to solid tumor indications with the benefit of the economies of scale associated with allogeneic cell format. 

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