Humane Therapeutics Through Crosslinking

A closer look

Our Technology

 
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The mechanism

How It Works

 

Step 1

An antibody fragment is attached to a DNA-like molecule (MORF1) to create a targeting scaffold (Fab’-MORF1).

 

Step 2

Fab‘-MORF1 is injected into the bloodstream to bind the target receptor on the malfunctioning cell.

 

Step 3

A polymer is attached to multiple MORF2s (P-MORF2).  MORF2 is complementary to MORF1.

 

STEP 4

P-MORF2 is injected into the bloodstream and attaches to multiple Fab’-MORF1 at the cell surface. This causes target receptors to crosslink. Binding of P-MORF2 to Fab’-MORF1 is the therapeutically active step. Fab'-MORF1 can be premixed with P-MORF2 prior to administration, if required. 

We can crosslink more than 10 receptors with greater efficacy resulting from more crosslinking. Multiple mouse studies have shown long term, curative survival. (Tested in xenograft SCID mice targeting CD20 in Raji cells.)

 

STEP 5

Crosslinking of cell receptors sends a signal downstream to engage pathways within the cell. These signals can cause cell suicide or immune system activation..

In the case of the CD20 receptor, crosslinking causes suicide of target B-cells with indications in Non-Hodgkin’s Lymphoma, Multiple Sclerosis, and Rheumatoid Arthritis.

REFERENCES

Drug-Free Macromolecular Therapeutics – A New Paradigm in Polymeric Nanomedicines (2015)

A Two-Step Pretargeted Nanotherapy for CD20 Crosslinking May Achieve Superior Anti-Lymphoma Efficacy to Rituximab (2015)

Drug-Free Macromolecular Therapeutics Induce Apoptosis of Patient Chronic Lymphocytic Leukemia Cells (2014)

Cell Surface Self-Assembly of Hybrid Nanoconjugates via Oligonucleotide Hybridization Induces Apoptosis (2014)

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