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The key to it is the GI50 value for the pancreatic (PDAC = pancreatic ductal adenocarcinoma) cell lines (first image) and the liposarcoma (STS) cell line (second image).

GI50 (Growth Inhibition 50%) is the concentration of a compound, such as a drug, required to inhibit the growth of cells by 50% in in vitro studies. It is a critical metric in cancer research and pharmacology used to evaluate the potency of compounds that stop tumor cell proliferation, often used for cytostatic agents. The lower the concentration, the higher the potency.

For the two PDAC cell lines the GI50s were 47.3nM and 54.9nM.

For the liposarcoma cell line, with AVA6000 alone the GI50 was 29.0nM and in combination with an ATR inhibitor, M4344 (aka gartisertib), was 6.9nM, i.e. even more effective.

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This is the abstract for the poster presentation: https://aacrjournals.org/cancerres/article/86/7_Supplement/7173/780950 , and these are the results given there:

"The GI50 of AVA6000 in two pancreatic cancer cell lines ASPC-1 and Mia-Paca-2 in the co-culture system with PSCs was 58±21.4nM, (Stdev,n=3) and 66.5±16.3nM (Stdev, n=3). No GI50 was obtained in both cell lines at the highest concentration of AVA6000 studied in both cell lines (>100nM n=3) if PSCs were not included in the culture. In addition, we demonstrated that the FAP inhibitor talabostat at 100µM reversed any growth inhibition by AVA6000 (highest concentration of AVA6000 tested 100nM) confirming AVA6000 activation was FAP dependent. We further studied the growth inhibition of AVA6000 in the liposarcoma cell line SW872-GFP in co-culture with FAP expressing fibroblasts GI50 30.6±6.7 nM (StdevD, n=4). The GI50 of AVA6000 was not achieved in the absence of fibroblasts at >100nM and the FAP inhibitor talabostat reverses this growth inhibitor effect in the co-culture system. The combination of AVA6000 and BAY1895344 in the co-culture yielded a 2 fold shift in GI50."

The GI50s in the two PDAC cell lines are different! 66.5±16.3nM and 58±21.4nM respectively. Odd?

The GI50 in the liposarcoma cell line is 30.6±6.7nM (so very similar to 29.0nM) and in combination with another ATR inhibitor, BAY1895344, the GI50 is only mentioned as "a 2 fold shift" (so something like 15nM).

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And all this means It Works™ and works even better in combination with ATR inhibitors, agents that prevent tumour cells from repairing DNA.

There is another risk with every new candidate when it first goes into humans opti and that's that it or a leaving group (such as the capping group or a self-immolative linker) or a degradation product — and remember that nearly all of these will never have been seen before by a human body — will cause a bad reaction of some kind. That is why the inital dose will be set low, below the danger threshold of the warhead. However, after the first patient has been dosed and the PK done they will have a clear idea of, outliers excepted (and findingn them is part of the purpose of the mass numbers Phase 3 trials), whether the whole caboodle is working as it should. Given CC's demeanour some three weeks post-first dosing I think it's fair to say AVA6103 is 'safe' within the parameters of what can be determined thus far.

These points are drawn together in a neat summary at the end: Section 12 (Investment Verdict & Summary):

"STRUCTURAL BUY

"Clinically validated platform priced as unproven concept — the discount to intrinsic value is structural, not speculative

"There is an important distinction between a speculative investment — where you are betting that an unproven concept might work — and an undervalued investment, where you are buying a proven asset at a price that does not reflect what has already been demonstrated. Avacta sits firmly in the second category. The pre|CISION® delivery mechanism has been validated in 63 human patients producing a 100:1 tumour-to-plasma ratio. The safety profile has been confirmed clinically — no maximum tolerated dose at 4× conventional doxorubicin dosing, with the FDA removing the lifetime cap entirely. The payloads are established cytotoxics with decades of data. And as of April 21 2026, AVA6103 has demonstrated activity even in very low FAP tumours, formally expanding the addressable population beyond the already-large FAP-high segment.

"This is not a bet on whether the science works. The science works. This is a bet on whether the market re-rates a proven platform from its current ~£349M valuation toward the $1–5bn range that comparable validated drug conjugate platforms command. The risk is financial — dilution, partnership timing, cash runway — not scientific. And financial risk at this stage is considerably more manageable than the binary clinical risk that "speculative" implies. The 10-indication addressable market, the compounding de-risk curve across successive programmes, the Science Day on May 6, and the H2 2026 AVA6103 clinical data all represent catalysts that could close the gap between current price and intrinsic value. At ~77p versus analyst targets of 81–99p and a base-case rNPV of 110–220p, the current price represents an anomalous discount to a platform whose core scientific proposition is no longer in question."

This detailed and interesting report was brought to our attention by gmcc:

Avacta Therapeutics: pre|CISION® Platform • FAP-Targeted Oncology • Investment Analysis

https://storage.googleapis.com/avacta-analysis/avacta_deep_research.html

I reproduce here Section 10 (Risk Assessment — Platform-Calibrated Model) which lays the '~25–30% (or even 5%) probability of success from Phase 1' to rest:

"Why Standard Phase 1 Risk Models Overstate Clinical Risk Here

"Conventional biotech risk models apply ~25–30% probability of success from Phase 1 to approval because most drugs fail for one of three reasons: the mechanism of action doesn't work in humans, the safety profile is unacceptable, or the drug doesn't reach the target at therapeutic concentrations. For Avacta, all three of those failure modes have been substantially de-risked by existing clinical data:

• Delivery mechanism — PROVEN IN HUMANS. FAP cleavage producing 100:1 tumour-to-plasma ratio is observed clinical data in 63 patients, not a hypothesis. The hardest question in this drug class — does it concentrate in the tumour in humans? — is definitively answered.

• Safety — VALIDATED CLINICALLY. No MTD at 4× conventional doxorubicin. FDA removed the lifetime cap. Cardiac toxicity — the primary safety concern for doxorubicin and the reason patients are excluded from treatment — has been eliminated in clinical practice.

• Payload activity — NOT IN QUESTION. Doxorubicin and exatecan are established cytotoxics with decades of clinical data. The payload mechanisms are not experimental. The only question was whether pre|CISION® could deliver them safely at therapeutic concentrations. It can.

• Platform compounding de-risk. Each successive programme narrows the remaining uncertainty. AVA6000 proved the delivery mechanism. AVA6103 adds one incremental question: does the Gen 2 sustained-release linker behave as expected in humans? AVA6207 adds: can two payloads be released simultaneously? Each is a narrower, more specific question than "will this drug work at all?" — which is what standard Phase 1 risk models price for. Today's AACR data showing AVA6103 activity even in very low FAP tumours further compresses the remaining efficacy risk."

Thanks. That's a very detailed and interesting report, particularly the bits towards the end.

If that's AI-generated then it's a good job, although I'd take issue with BOTH of AVA6207 and AVA7100 being Gen 3 pre|CISION. AVA7100 is Gen 3 (AffDC) but I'd say AVA6107 is an extension of Gen 2 (sustained-release PDC).

I found the 'Hidden Signals' (Section 11) the most interesting. Well Signals 01 to 05 anyway. I think AVA3997 (Signal 06) is dead in the water (novel so an untried and -test cytotoxic, effectively almost out of patent life) as, with the new chemistry that can link 'almost' any drug to the didpeptide, out-of-patent bortezomib itself must surely now possibly come into play. Signal 07 (Increased IP Filings) is, I think, rather unnecessarily speculative — another patent filing could be the specific AVA6103 structure, as that will need to be specifically defined and protected.

There's also a neat summary at the end (Section 12):

"STRUCTURAL BUY

"Clinically validated platform priced as unproven concept — the discount to intrinsic value is structural, not speculative

"There is an important distinction between a speculative investment — where you are betting that an unproven concept might work — and an undervalued investment, where you are buying a proven asset at a price that does not reflect what has already been demonstrated. Avacta sits firmly in the second category. The pre|CISION® delivery mechanism has been validated in 63 human patients producing a 100:1 tumour-to-plasma ratio. The safety profile has been confirmed clinically — no maximum tolerated dose at 4× conventional doxorubicin dosing, with the FDA removing the lifetime cap entirely. The payloads are established cytotoxics with decades of data. And as of April 21 2026, AVA6103 has demonstrated activity even in very low FAP tumours, formally expanding the addressable population beyond the already-large FAP-high segment.

"This is not a bet on whether the science works. The science works. This is a bet on whether the market re-rates a proven platform from its current ~£349M valuation toward the $1–5bn range that comparable validated drug conjugate platforms command. The risk is financial — dilution, partnership timing, cash runway — not scientific. And financial risk at this stage is considerably more manageable than the binary clinical risk that "speculative" implies. The 10-indication addressable market, the compounding de-risk curve across successive programmes, the Science Day on May 6, and the H2 2026 AVA6103 clinical data all represent catalysts that could close the gap between current price and intrinsic value. At ~77p versus analyst targets of 81–99p and a base-case rNPV of 110–220p, the current price represents an anomalous discount to a platform whose core scientific proposition is no longer in question."

Do you mean the 'Load More' glitch where some just previous posts may someties not get loaded so appear to have been deleted?

ToucanOfDoom, you continually snipe insults at posters here and then wonder why you are called a twat...

Well the signs of a possible peak were there yesterday. I'm not a chartist by any means, I'd just say it could go up or down from here or bobble along for a while. However we've got Science Day coming up in a couple of weeks so expect a rise in expectations — and frenetic ramping by the uber-ramper formerly known as monkeyspanker — ahead of that.

Faridox data will be presented here, at ASCO, https://www.asco.org/abstracts-presentations/264652

^Came here

I'm the same as you PL75. Change here for the LFT, stayed when I saw they had the holy grail.

All that's as may be but the fact is that traders do use charts and RSI in lieu of understanding the underlying investment and it's probably wise for oneself to understand what forces are moving the share price — and we know that Avacta has been, and very largely continues to be, a plaything of the traders.

I was wrong earlier. Enhertu has patent protection until around 2033 (main patent) to 2035/6.

Now, with the last (15 minute delayed quote) share price at 80.38 (a buy), the 14 day RSI is 70.14 and 7 day RSI is 82.29. Traders will surely be soon starting to think about taking a profit if this rise continues.

RSI has been steadily moving towards overbought territory. Currently 68.58 (on the 14 day measure) and although it can go a lot higher, up towards 100 with frenzied buying (which we don't have at the moment), 70 is usually taken as the start of the trigger to sell. On the 7 day measure the RSI is 80.26.

I'll not be trading any until the share price is a lot higher and unless the RSI is crazily high. I think that with the possibility of news at any time now being out, even a bit, in order to try to make a few quid/reduce my average by fractions of a penny or to gain a few extra shares is too big a risk at the moment.

ToucanOfDoom will be all over this.

Drugs get compared all the time. I took it to be a clarion blast as a wake up call to all ADC developers and to AZ/Daiichi in particular as owners of a soon to be out of patent key income generator.

This is a Phase 1a study, so that means safety and tolerability first and foremost. It also starts with a low, intentionally sub-lethal dose level (just in case – no one, not Avacta, nor the clinicians, nor the trial site management, nor the FDA want to take any risks with patients' lives).

So if the purpose is to gather safety and tolerability data rather than show efficacy it is as well to spread the net wide. As they are focussed on indications they want to take forward in Phase 1b they could be increasing the number of indications now (if indeed the expanded indications relates to Phase 1a and not 1b) in order to gather efficacy data, of which there will be some, during this phase.

"Ironic given Avactas link up with tempus haha"

What Temps seem to do is number crunching and pretty displays. There is more behind it than that of course such as what data are collected and how the data are linked and the company may offer other capabilities but what AVACTA seem to be using it for is fast data analysis that can be done in seconds rather than man months.

AI does have its uses as an encyclopedia (definitions and explanations of well characterised entities) but is very dodgy when it comes to interpretations and poorly defined or covered entities. It is also not necessarily comprehensive, failing to cover patents for competitive intelligence for instance.

Unless you are looking for hard facts, use AI with caution and compare what it returns to what you already know and understand about the topic. Do not go into a topic asking for an interpretation of something you know nothing about and expect to be taken seriously when you then post it on a forum.