@Gan_Gans YOU ASKED FOR IT LOL A number of weeks ago when there...

@Gan_Gans

YOU ASKED FOR IT LOL

A number of weeks ago when there was all the talk of other indications patents etc and I took a bit of time out from the forum.

I did a little digging looking for patents on other indications as I suppose @George1972 had done in the past

I saw Georges previous post but we must have been searching slightly different avenues, I presume George may have been searching CD49d and came up with the blood report

he did ask for opinions but no one really followed up, apologies George but at the time i came acoss this info, I had, had a gutful of the garbage going on in the forum and decided to give things a miss for a while

However slight change of thought process now

So @Gan_Gans

I will share what I think is IMHO,

or should I say IMHO could well be classed as Market sensitive information, as I have actually heard nothing from the company on this, and apologise if I have missed it for some reason or if my train of thought is completely out of context, along with a complete misunderstanding and misinterpretation of what I have read

But as George Said this could open the door to another multi billion $ avenue emerging

So here goes

First up I would like to take you back to december 2015 whereby as one can see

ATL1102 Cancer Data Presentation looked to be a pretty big deal as in,

it had a full presentation of its own in an

ASX ann see below

8th December 2015

ATL1102 Cancer Data Presentation

Antisense Therapeutics Limited (“ANP”

wishes to advise that data from the testing of ATL1102 in an animal cancer research study conducted at the Children’s Hospital Los Angeles (CHLA) is to be presented today at The American Society of Hematology (ASH) 57th Annual Meeting in Orlando Florida.

The data from this pilot animal study shows that ATL1102, an antisense drug targeting CD49d (VLA4), led to the rapid mobilization of acute myeloid leukemia (AML) cells to the peripheral blood in mice that had been engrafted with human AML cells.

Details of the study and results are outlined in the attached poster presentation.

A new provisional patent application incorporating this data and covering ATL1102’s potential application in AML and other leukemias has been filed by ANP.
The rationale for this study of ATL1102 is based on the bone marrow microenvironment having been shown to promote cell adhesion-mediated drug resistance in leukemia cells. Breaking the adhesive bonds of AML cells with their protective niche to mobilize them from the bone marrow to the peripheral blood may make drug treatment more effective.

Studies have suggested the adhesion molecule CD49d is an anchor molecule for AML and certain other leukemia cells in the bone marrow and that drugs like ATL1102 which reduce CD49d expression may cause the release of these cancer cells from their protective environment to make the cancer cells more accessible to chemotherapy.

No drug targeting CD49d is currently approved for use in leukemia. AML is the most common acute leukemia in adults and the seventh most common pediatric malignancy comprising approximately one-fifth of pediatric leukemias.

Treatment is dominated by generic chemotherapeutic drugs. In children, relapse following primary chemotherapy approaches 40%, and the 5-year event-free survival rate is only approximately 50%. Novel therapeutic strategies are highly warranted to eradicate residual disease.

Further animal studies are ongoing at the CHLA at their cost to more fully assess ATL1102’s therapeutic potential in this disease setting.

Contact Information: Website: www.antisense.com.au Managing Director: Mark Diamond +61 (0)3 9827 8999

So it can be seen from the above that ATL1102 mobilises AML cells




see extract from what looks to be a further study published in 2017

Abstract

mce-anchor We recently demonstrated the effectiveness of blocking CD49d with anti-functional antibodies or small molecule inhibitors as a rational targeted approach to the treatment of acute leukemia in combination with chemotherapy.
Antisense oligonucleotide promises to be no less specific than antibodies and inhibitors, but more interesting for pharmacokinetics and pharmacodynamics.
We addressed this using the published CD49d antisense drug ATL1102. In vitro, we incubated/nucleofected the ALL cell line Kasumi-2 with ATL1102. In vivo, immunodeficient hosts were engrafted with primary ALL cells and treated with ATL1102. Changes in expression of CD49d mRNA and CD49d protein, and of cooperating gene products, including ß1 integrin and CXCR4, as well as survival in the mouse experiments were quantified.
We observed dose-dependent down-regulation of CD49d mRNA and protein levels and its partner integrin ß1 cell surface protein level and, up-regulation of CXCR4 surface expression. The suppression was more pronounced after nucleofection than after incubation, where down-regulation was significant only at the higher doses. In vivo effects of ATL1102 were not sufficient to translate into “clinical” benefit in the leukemia model.
In summary, antisense oligonucleotides are successful tools for specifically modulating gene expression but sufficient delivery to down-regulate CD49d in vivo may be difficult to achiev


So I think Georges post was shrugged of because it has been covered before because of the statement above

ATL1102 were not sufficient to translate into “clinical” benefit in the leukaemia model.



So to move on I drilled down into this to see why the patent had been extended and BINGO on the

22/06/22 the below patent was granted for mobilising Leukaemia Cells

Nothing new here you may say same old same old from 2015 we are aware that ATL1102 actually mobilises Leukaemia Cells

So lets dig a little deeper into what has actually been ongoing studies and what do we uncover



U.S. patent number 11,041,156 [Application Number 15/971,938] was granted by the patent office on 2021-06-22 for mobilizing leukemia cells. This patent grant is currently assigned to Antisense Therapeutics Ltd, Children's Hospital of Los Angeles. The grantee listed for this patent is Antisense Therapeutics Ltd, Children's Hospital of Los Angeles. Invention is credited to Yong-Mi Kim, George Tachas.



From what I can make of this as a Layman and this is just my interpretation only, I could be totally wrong in my assumption and again this is just IMHO

A problem with treating Acute Myeloid Leukemia ( AML ) is the fact that the Leukemia cells hide in the bone marrow of the sufferers and it makes it difficult for the Treatment ARA-C Chemo to reach its target cells

But when treated with ATL1102 it would appear that Atl1102 EITHER KILLS OR FLUSHES THESE CELLS out of hiding from the bone marrow and into the blood stream whereby the Chemo can do its job more efficiently


See Below from the actual report partial out,takes

Results
[0270]
ATL1102 can efficiently decrease CD49d expression in AML cell line in vitro and in vivo, and ATL1102 leads to mobilization of AML cells to the peripheral blood.


[0278
In the bone marrow (BM—FIG. 11 left hand column) there are fewer human (hCD49d+) AML cells in the ATL1102 and Ara-C combination compared to the Ara-C mono therapy (i.e. 70% vs 30%).

This suggests they have been released from the bone marrow or do not survive in the bone marrow because of ATL1102 treatment, consistent with mobilisation of these cells from the bone marrow/or apoptosis ( CELL DEATH ) of these AML cells

(see also FIG. 13). Thus in some embodiment's, the ATL1102 treatment sensitises the AML cells to clearance by Ara-C. The cells that were still in the bone marrow expressed substantially less hCD49d (i.e., 800 vs about 450 MFI) suggesting good CD49d target knockdown. This was more pronounced in the peripheral blood (PB). In the spleen there is no difference in % of human AML cells, but the cells in the spleen appear to express more hCD49d. In the liver there are no differences in either % or MFI.


[0279]

FIG. 12A-C illustrate the survival of the different groups as the data became available. In each graph, there was a statistically significant increase in the survival of the combination treatment group compared to Ara-C treatment alone. Overall, there was a significant 12.8% increase in the median survival in the combination group relative to the mono-therapy.


[0280] An experiment was also conducted to evaluate mobilisation of en-grafted human U937 AML cells (expressing hCD45) in tissues over 24 hours after ATL1102 and AS control administration in male NSG mice on day 24 after engraftment. As shown in FIG. 13, bone marrow has 10-25% human CD45+/AML cells (i.e. vs 75-90% mouse CD45+ leukocytes), the liver has over 90% human CD45+/AML cells, and in the spleen <5% with no significant differences in AS control vs ATL1102 mice at baseline or 24 hours post 150 mg/kg dose. There is, however, with the control AS a significant increase in AML cells in PB at 24 hours vs baseline to ˜2% AML. In contrast there is only 1% AML cells in peripheral blood treated at 24 hours with compared to ATL1102 treated animals, and no significant increases vs baseline. AML cells could be expected to move from tissues to the PB within 24 hours of dosing as occurs with control AS. In the control there was a statistically significant increase in the % of AML cells in the peripheral blood at day 4 vs baseline,

but not in the ATL1102 treated group. This indicates U937 cells treated with ATL1102 show reduced survival in the blood.

U937 is a pro-monocytic, human myeloid leukaemia cell line


So you guys tell me is this a gross misinterpretation on my behalf

or would you say that looking at the result and coinciding ASX ann from way back in 2015

which was in actual fact presented and classed as ATL1102 Cancer Data Presentation


WOULD this latest information have deserved better than what we were dished up below


WHAT WAS STATED IN THE STATUTORY ACCOUNTS ASX ANN 25/08/2021


US patent 11041156 has been granted and is in the process of being registered covering the use of ATL1102 for mobilizing leukemia cells in the treatment of acute myeloid leukemia (AML) to 2036


Is this good enough you tell me

Would the next step be a PH1/2 AML Clinical trial in humans ?

ENJOY Gan_gans

SEE HOW WE GO