Member Info for Haywain

It is that JHFH but there are different ways of achieving this - it’s about how to deliver the genetic information necessary to the body’s t-cells such the ability for the cell to manufacture and express anti-FLT3 ScFv is conferrred - many ways to skin a cat : 1. Lipid nanoparticles (LNPs) – mRNA delivery

2. Direct viral vectors – AAV or lentivirus

3. Antibody-targeted nanoparticles – e.g., anti-CD3/CD5/CD7

4. In-vivo transposon systems – Sleeping Beauty, PiggyBac

5. Engineered immune-tropic / oncolytic viruses

6. Programmable synthetic immune receptor systems (CAR-like, switchable, mRNA-based)

It’s why autologous is better - for efficacy and safety just a bit cumbersome on the logistics side to have to perform leukapheresis, transport samples, manufacture CAR-T and transport back to the clinic- which is why they are trying to develop “off the shelf” versions of Car-T which allo, and in-vivo are : but with other challenges to combat

The problem with Allo is GvHD - you can knock it back with gene editing but you can’t eliminate it - body recognises the T-Cell as non-self and rejects is

Actually their patent on the anti-FLT3 ScFv covers them for the following indications - you can only assume that they see potential benefit in these also : ncluding all major leukaemias (AML, ALL, CLL, CML), aggressive and indolent lymphomas (including Hodgkin’s, non-Hodgkin’s, DLBCL, follicular and T-cell), multiple myeloma, neuroblastoma, severe inherited and acquired bone-marrow failure syndromes (including sickle cell, beta-thalassaemia, Diamond-Blackfan anaemia, aplastic anaemia, MDS, Fanconi anaemia, PNH and congenital thrombocytopenias), as well as life-threatening immune disorders such as SCID.

Well there are limits - obviously the cancer would have to express FLT3 which limits it to myeloid linaege cancers - but I belive there is a case for BPDCN, ALL and others but it would be the FLT3 high subset of these patients. As an aside if you think in-vivo CAR-T is the future what you are really saying is that CDX is the future because it is essentially in-vivo HG-CT-01 : an off the shelf version. also because we wholly own our IP pretty easy to make an mRNA construct of our own HG-Ct-1 and also have an in-vivo CAr-T : but why would we when we are demonstrating efficacy with HG-CT-1 currently in the clinic?

Just as monoclonal antibodies were a step up from small molecules, more selective and designed rather than as a result of library screening, bispecific antibodies , ADCs where a step up, cell therapy is a step up, in-vivo is the new sexy thing and is a step up in terms of logistics - not in terms of efficacy. What you actually see is a now eco system where all of these things live together. There is always space for good science no matter what the modality - you can even take a 50 year old chemotherapeutic agent and make it less cytotoxic and more targeted and apparently that can garner a huge investor base. Good science is good science - I invested in hemogenyx because they have taken good science to the next level - it is not about incremental improvement they are trying to provide a “curative” option to patients that currently don’t have one - including paediatric population.

Says the man who doctored the content of the prospectus to put your own little spin onto it - Doesn't really pass the red face test does it ?

Soon didums

Soon didums

Comment - nice try : Gallop’s LYT-200 update is fine as far as small-molecule/immunomodulators go but it highlights just how exceptional HG-CT-1 actually is. LYT-200 shows ‘favourable tolerability’ with median OS of ~13 months in combination with SOC and in patients who can still tolerate therapy, i.e. a population far fitter than r/r AML patients sent for CAR-T. The key point: their responders still needed transplant to consolidate. HG-CT-1 is clearing blasts as a monotherapy in patients who were refractory to everything and were not even transplant candidates with zero CRS/ICANS and emerging long-term remissions of 6–11 months already. LYT-200 is incremental; HG-CT-1 is potentially transformative. One shifts survival curves; the other may actually replace salvage chemo and HSCT for FLT3+ disease if replication continues.

Let’s Gallop to niche marginal incremental improvement - Yawn

By all means be cautious and do take the time to do a bit of background reading on the subject and try to compare apple with apples - same indication/ modality is a good starting point - CAR-T and AML

And I have just pointed out that even in disaster situation the asset value of what hemogenyx have developed is significantly more than the market cap - so you can forgive me in brushing aside your faux concern. I absolutely want to support the company in any way I can because they are doing remarkable things. The fact that HG-Ct-1 could be curative in an indication where for so long so little hope has been offered to patients is remarkable - and does not deserve parasitic trolls like you.

That all the warnings are true and that the London market is so diabolical that it can not support funding 5-6M for another year of progress and Hemogenyx goes into administration Hg-CT-1,CdX and CBR are sold by administrators in fire sale to the highest bidder -in that disaster scenario - the value of HG-Ct-1 alone still represents multiples of the current market cap. The share price is irrational and we find our selves here because of fear and manipulation on the back of warrant sellers who don’t care what they are invested in flipping for a few quid . No first in human CAR-T with any demonstrable efficacy has ever sold for less than 100M- let alone one for r/r AML - that’s a fact. And there would be competing pharma interest for this without doubt.

So let me get this straight - you accuse JHFH of selling at the top at the expense of other shareholders- and then you say that’s what he should have done heading your advice ? Just an oxygen thief.

I have never mislead - just countered the deliberate and repeated mistruths that have been posted here- what I have said is what I believe : otherwise I wouldn’t have said it.

Avacta and Hemogenyx are not comparable in terms of regulatory expectations or timelines. Avacta’s platform is a novel chemical modality, so big pharma naturally want long multi-year datasets before committing. CAR-T however, is an already validated class with multiple FDA-approved products and a well-defined regulatory pathway. What’s novel in Hemo’s case isn’t the technology itself but the target (FLT3) and the unexpectedly strong clinical performance as demonstrated by durability and CR in initial dose cohort as well as FDA greenlighting paeds after data from 2 patients —Regulators and BP don’t need five years of Phase 1 to “understand the mechanism” because CAR-T is a mature field with established safety and efficacy benchmarks. In practice, dose-escalation CAR-T studies typically run 12–18 months - only delayed here because of finances. When early patients show deep durable remissions without ICANS/CRS which I suspect is the case here -development accelerates, not slows. So while both companies are innovative, the idea that Hemo faces the same acceptance barriers as Avacta simply isn’t correct: the risk profiles, mechanisms, regulatory frameworks and partnering dynamics are fundamentally different.

My view is that it is worth multiples and that is exactly why it has been attacked and Aldebaran was able to forward the details of that attack to the market - you get a bigger chunk of the company if you force the share price as low as it can be before you do a financing deal - an attempt at predatory financing is my best guess - alternatively you can believe that Aldebaran is exceptional at reading charts - almost visionary -but for some reason he spends hours a day across months posting incessantly on LSE instead of enjoying his life with the millions he is obviously capable of generating with such chart reading capabilities.

That’s not what I said Beunavista - read it again : I said curative signal - if that curative signal carries on people will talk about HG-CT-1 being curative much in the same way that they talk about bone marrrow transplant being curative currently- though hopefully in a greater subset of patients. It’s actually mechanistically works in much a similar way to HsCT - graft-vs-leukaemia is the name of the effect and it is actually the CD8 t-cells that are generated by the graft that cause the durable response through clearance of the quiescent leukaemic progenitor compartment - guess what HG-CT-1 is an anti-FLT3 directed CD8 T-Cell (as a reminder FLT 3 is ubiquitously expressed on both bulk blasts and leukaemic progenitors)

Far from what your moniker would suggest - it is not a good look.