$10 Billion Deal, page-11882

MM = Has participated along with all the other directors in their full entitlement in the last CR great leap of faith they have their money where their mouth is.

MM has been working and enhancing BIT225 over the last 20 years.

MM dropping statements such as

MM mentioning we looking forward to the new year with confidence. along with 'we believe BIT225 is close to the finish line '

If people read what MM has provided in a previous report below you wont be taking BIT225 lightly.

One of the main problems in trying to cure HIV is the
nature of the immune cells the virus infects. Its major
target is a type of white blood cell known as the CD4 cell
that has several important roles in the immune system.
These include marshalling immune responses to attack
foreign agents such as viruses and “remembering”
previous infections.

Subsets of CD4 cells can, in effect, store a record of
known infections, but the problem is that that these cells
can become dormant and live in the body indefinitely.
Once these cells are infected with HIV, the virus can
continue to survive in the body by hiding in these
dormant CD4 cells.

Other cells, such as macrophages, are also targets for
HIV-1 infection. Virus in these macrophage cells as well
as in the dormant CD4 cells is hidden from the immune
system meaning that anti-HIV drugs can never truly
eradicate the infection from these reservoirs. Patients
infected with HIV-1 must remain on treatment for life.
In March, we reported that Biotron had discovered a way
for these hidden HIV-infected cells to be found, allowing
the immune system to attack and kill the virus.

We conducted a Phase 2 randomised placebo-controlled
clinical trial on 36 HIV-1 infected patients in Thailand in
which we tested BIT225 in combination with Atripla, an
approved current anti-HIV drug (ART). As reported to the
market in late 2018, we saw unexpected, unique changes
in the profiles of key immune cell populations in the
BIT225 + ART group