Gordon Stein, CFO of CleanTech Lithium, explains why CTL acquired the 23 Laguna Verde licenses. Watch the video here.
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Can you qualify ehybyou say that live data. What impressed you about her in the video?
CC really is a breath of fresh air
Sorry @ Saint68 for providing the link .
@Doggy100 Many thanks for sharing
Nicely fits with this article : Avacta chemists addressing the the right things .
https://www.aacr.org/blog/2024/01/31/experts-forecast-2024-part-4-cutting-edge-tech-for-oncology-drug-discovery/
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"New therapeutics can be a driving force in extending patient survival and reducing deaths from cancer. Last year alone, the U.S. Food and Drug Administration (FDA) approved 17 new cancer drugs and expanded prior approvals for several others.
Despite this progress, drug discovery still has a long way to go, said Paul Workman, PhD, a professor and drug discovery expert at The Institute of Cancer Research in London.
“Ninety-five percent of cancer drugs tested in clinical trials never get approved,” he said. “This is because they end up being too toxic, ineffective, or no better than existing therapies once they are evaluated in patients, despite promising preclinical data.”
Paul Workman
Paul Workman, PhD
Moreover, only 14% of cancer patients in the United States are treated with precision medicine, and only 7% benefit—a sobering reality that Workman attributes in large part to the limited number of cancer drivers that are currently druggable. “The main reason for the low application of precision medicine is that most cancers are driven by genetic alterations for which we currently have no drugs.
“So, number one, we need to increase the clinical success rate of the drugs we are developing, and number two, we need to find ways to discover drugs against the so-called ‘undruggable’ targets,” he said. “In addition, we need to use intelligent combinations of new and old drugs to overcome drug resistance.”
Before new small-molecule drugs can reach the clinic, they must be designed to selectively block the function of the desired target protein and undergo extensive testing in the lab. This relies on researchers being able to identify new targets and engineer compounds against them that are safe and effective.
“This is where new technologies will help us,” Workman said. In 2024, he predicts that rapid advances in artificial intelligence (AI), chemical technology, and small-molecule chemical probes or tools will provide the cutting-edge resources needed to expand and accelerate drug discovery for cancer. "
Here’s the first clown 🤡
That's where all the placing money goes! Video productions!!
Oh dear oh dear!!!
Let’s see which trolls try to talk that video down
Just watched it
Very good
Drink up trig were on a winner!!
New video just been release :
https://twitter.com/avacta/status/1783492089428263107
Its always been a p&d stock for insiders!
Ask Sir Al he got a house out of it!
"Welch", "loosing"?
Really? - get spell check program if you can't spell yourself.....
Check a dictionary too - welch has a completely different meaning to Welsh!
Still a neanderthal, obviously.
If that were true thrn he wouldnt need 4M options all which genetate him a massive payoff even at todays SP.
Board needs to realign benefits for him, CFO and if we have one thats awake Chairman to share holder value. Forva start ATH would be minimum for any new options
Y tee. A man with limited vocabulary?
His “ oh dear, oh dear” comments repeated here for the umpteenth time and also twice today on the TERN board.
Spelling not to good either- what does “loosing money” mean?
Touk, it’s not a dilution that’s taking place. That would mean the the mass of drug has remained the same and blood volume has increased.
So the Pt1/2 of AVA6000 is going to be caused by its breakdown at the TME (good), breakdown throughout at non cancer sites (bad), and clearance of AVA6000 by kidneys or liver (good as long as no toxicity). All drugs have to be removed from the body - one way or another. So if the t1/2 is mainly because of FAP breakdown of AVA6000 at the TME, this is actually a good thing.
Also biopsies are of course are taken by different people and even with normal doc will have variables with the same dose as we are all different. An important take away is you can see a correlation between dose and dox. Higher dose higher dox. Yep it works as it should.
Welch clearly loosing money here
Oh dear oh dear
"On 25 April, World Malaria Day 2024 will be marked under the theme “Accelerating the fight against malaria for a more equitable world”
Scroll / Check out all the LD Malaria Solutions products
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Touk, given the following thresholds for the various mechanisms of action of dox:
DNA adduct formation 25nM
Free radical formation/cardiomyocyte apoptosis1 100nM
Topoisomerase Inhibition1 400nM
And that DNA adduct formation is the mechanism of action that provides the greatest effect in reducing the tumour size, and that the range discovered in tumours was 76-2310, it suggests there is sufficient dox getting into the tumour, and all but 2 of the biopsies exceeded all the threshold above.
Now it would be good to have a chart which demonstrated the efficacy of dox (at least in average terms) against values from these thresholds and above. This would really put the argument to bed. I have had a scour around but cannot actually find any relevant data - as AS himself stated was the case a while back.
1. AVA6000 exhibited rapid distribution, with a half-life of 45 minutes backing up my assertion that dilution in the bloodstream is too rapid.
Comedy gold 😂😂😂😂😂
Doxorubicin, a frontline drug used in cancer treatment, has been employed for over 30 years. While it can cure certain cases, it also poses toxicity risks to major organs, particularly life-threatening cardiotoxicity. This toxicity necessitates dose-limiting treatment1.
Here are some key points about doxorubicin distribution:
Initial Distribution Half-Life: Approximately 5 minutes, indicating rapid tissue uptake.
Terminal Half-Life: 20 to 48 hours, reflecting slow elimination from tissues.
Seriously will stick with the case studies and real life result’s, than pay attention to Touk the Sunday scientists analysis. Only takeaway he should be involved with is the pensioners fish and chips on a Friday.
For me this is the clearest analysis of trial results. An excellent article but my takeaways are:
1. AVA6000 exhibited rapid distribution, with a half-life of 45 minutes backing up my assertion that dilution in the bloodstream is too rapid.
2. Tumor biopsy data demonstrated a mean concentration of doxorubicin in the TME of 860 ng/gm (range 76-2310 ng/gm, n=9). Which leads me to believe that there needs to be a lot of work done on targeting patients and dosing regime.
3. In contrast, blood samples collected at the biopsy showed a circulating free doxorubicin concentration of 8.3 ng/ml (range 2.4-15.9), indicating a higher concentration of doxorubicin in the tumor relative to plasma. Obviously supporting the conclusion that the platform works.
So we await the results analysis of arm2 to find out whether I’m selling my house to upsize or downsize 🤣🤣🤣. That’s a joke BTW.
13.27: makes the point. VGLA
"whot"?
Neanderthal.
Thats better!