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Like the notion selling diminished with flurries of upward jabs.
"the unintended events" are being reduced each day by
computational and experimental methods that are bringing researchers closer to their goal of revealing exactly where in a cell or tissue each gene is expressed.
DTIL: this guy has almost" stolen my thoughts:
https://stocktwits.com/schultzeee
DTIL 1.53.
Truth be told, I know nothing about the prospects of this stock to yield a net profit.
Insider selling and their funding principle to attract partners, capturing Lilly and Novartis and others already, with more insider buying from their top execs. tilts to me, a higher probable promise than suppositions I could surmise absent those facts.
The video (I linked) however suggests to me, that DTIL is the most promising scalable medical stock I can think of, even if true its ultimate success will lead to complete unfortunate failure.
The idea that this gene editing platform can conceivably be used to be effective for at least 7K diseases is crucial to proclaim its surpassing promise. The rapid new developments in new computational and experimental methods can avail foreseeing continuous increased effectiveness of this platform, even after periods of enduring inconclusive failure.
Bottom line: I can not recommend as a wise investment the stock DTIL,
But when I match DTIL against all possible investments in charitable enterprises, with the expectations of deriving no profit except tax benefits , I think DTIL is also eligible to receive a "philanthropic" donation, with no prospects of a return, except, to just be able to say, when asked to donate money for some disease, the words "I already gave".
Anyway,if anyone can name a stock with more promising scalable prospects than DTIL, it would to the highest degree, tease my curiosity.
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DTIL early success will allow DTIL to partner with others for the 7K diseases and allow them the honor of paying for all R and D.
DTIL: at different points in time, could see PR pin ball machine output as
this editing platform has so many explorational aspirational stabs towards enduring cures with an infinity of ways to enhance and modify their first tries with elite collaborative partners..
For example platform may be perfect but DNA edited into wrong target tissue spot, oops must try again this same platform.
DTIL:
DTIL: CART-T gene editing laboriously explained in this 2 hour video.
DTIL : Since Friday 72 hour+ blackout observed, only Swampboots could post on IHUB, regarding a stock which soared 23% today and has symbol DTIL, I deserve this exclusivity!
DTIL 1.77 a start!
DTIL 1.54 crumbs from offering completion PR.
DTIL: 1.44 price reflects a lack of exposing deep fraud and deception, or misdirection, in the face of these realities and theories:
1- price falling violently from 2 to 1.11 because of a false material influence of another T-Cart editing platform which failed (collateral damage from CRBU data).
2-- DTIL not desperate for cash with 100 million in recurring revenue, and market cap below 100 million, before their additional 50 million underwriting share offering..
3-- Novartis affirming and validating their platform with 75 million
divy and offering 1.4 billion potential milestones.
4- CEO upping his stake by 40% with 30,000 additional share purchase @$2, days ago.
5- 50 million dollar dilutive offering@1.39 throwing off scent to dumb money but ensuring cash runway to 2024.
My theory, a cynical attempt by group to attack share price who believe (correctly) they can capture huge shares for future ante, believing technical vol. price drops rule short term investing predilections, confirming to the mob, that the dictum do not fight the tape is usually the most authoritative source consistent with implementing prudent investing behavior.
Net effect to my brain is that this is a rare "no-brainer" which defies all rules I know about investing in a stock, and a cautionary note to myself not to invest in any BIo stock because I believe in its great science without evidence of massive insider buying and affirmation by one of the top largest pharmaceutical firms with a major investment and alliance.
DTIL 2.19 after hour spike on news I did not read sold.
DTIL: Note well
DTIL is no brainer, second after MICS alert a couple of weeks ago, and second after never finding a true live present one I was comfortable to declare.:
See this post which confirms:
https://investorshub.advfn.com/boards/read_msg.aspx?message_id=169114174
DTIL added 1.59 on "punk" downgrade to market perform.
From 10K:
Importantly, our one-step genome editing
approach avoids making multiple breaks to the T cell’s DNA and also contributes to minimizing cell processing time, which helps prevent the
CAR T cells from differentiating during the process.
• Novel co-stimulatory domain. Our genetically engineered CAR T cells incorporate a novel, proprietary, costimulatory domain called N6, which
may enable us to enhance cell proliferation and effector function while preserving cell phenotype. We engineered N6 to improve on the function
of the 4-1bb costimulatory domain commonly used in autologous CAR T products. Our preclinical data suggests that, compared to 4-1bb, N6
provides an activation signal to the CAR T cells that better preserves cell expansion potential while maintaining naïve cell phenotype following
exposure to cancer cells. We also believe N6 can help avoid CAR T cell hyperstimulation, which can contribute to adverse events seen with
autologous products.
This allows us to “fine-tune” the CAR T cells to ensure that they respond appropriately to the cancer but do not become
hyper-activated or exhausted. The below comparison demonstrates the difference in consistency achieved by using lentivirus delivery compared
with targeted delivery through an ARCUS nuclease. CAR T cells produced using ARCUS exhibit reduced cell-to-cell variability as well as more
controlled levels of CAR gene expression depending on whether the cells are tuned for high expression or low expression.
DTIL why weak after strong report today?
PR https://www.biospace.com/article/releases/precision-biosciences-provides-update-on-allogeneic-car-t-programs-and-path-forward-with-its-lead-pbcar0191-candidate-for-car-t-relapsed-patient-population/
Slides https://investor.precisionbiosciences.com/static-files/717d82d7-d304-4428-ba22-1a19c965d8d5
The most popular first salvage regimen for relapse or progression was an alternate CAR-T therapy (dual or alternate target) regardless of CD19 positivity. 27% of responders chose this regimen for CD19 positive relapse, while 31% of responders did so for CD19 negative relapse. 88.5% of responders favored consolidative allogeneic hematopoietic cell transplantation (alloHCT) after response to salvage, whereas 51.2% of physicians would consider autologous hematopoietic cell transplant (AHCT) in transplant naïve patients.
https://www.astctjournal.org/article/S2666-6367(22)01360-4/fulltext#.Yp5U3ghW7h4.twitter
Targeting PARP11 to avert immunosuppression and improve CAR T therapy in solid tumors
From memory, the ORR for PBCAR0191 plus eLD chemo was 100% (66% CR rate) and the response duration exceeded the original response to an auto product in three of five. If it holds up in a larger population a registration-directed PhII could happen.
There is also clinical data from patients with R/R DLBCL and R/R CLL, which shows a correlation with (durable) responses and the proportion of naïve and/or memory-like CD8+ T-cells.
Hopefully, the optimised manufacturing process (which the company has talked about) for PBCAR19B has allowed them to increase the phenotype(s) without the need for a new IND application.
As for the strategies outlined in that (and other papers) for increasing efficacy will be looked at by them as they could easily be incorporated into future trials.
Response MCL AUTO limited by:
1. T cells fitness and dose of CD8 and CCR71 CD45RA1 T cells too low.
2. High TB
P2 trial of the autologous anti-CD19 chimeric antigen receptor (CAR)
T-cell therapy brexucabtagene autoleucel (KTE-X19) in patients with heavily pretreated MCL. The median DOR was 46.7 months among patients with CR (46/71) and 2.2 months in patients with PR (16/71)
https://ashpublications.org/bloodadvances/article/4/19/4898/464200/Tumor-burden-inflammation-and-product-attributes
phase II trial of the autologous anti-CD19 chimeric antigen receptor (CAR)
T-cell therapy brexucabtagene autoleucel (KTE-X19) in patients with heavily pretreated MCL
The median DOR was 46.7 months among patients with CR (46/71) and 2.2 months in patients with PR (16/71)
https://ascopubs.org/doi/pdf/10.1200/JCO.21.02370#.YptkxkBhQis.twitter
“The CAR T relapse setting is a rapidly growing area with dire unmet medical need that is not adequately addressed by current treatment options.”
https://ascopubs.org/doi/full/10.1200/JCO.21.02370
These pharma execs didn't want to talk about allo. DTIL has shown T cells from a healthy donor beat exhausted T cells from the lymphoma pts. who relapsed on auto. Increasing the dose from 300 to 500 M should result in high CR @ 28 days.
For auto. Here is (AUTL's) Dr. Pule on so-called point-of-care
The company will share an update on its CAR-T programs during a company-hosted webcast and conference call on the 8th at 8:00 AM ET.
Efficient reprogramming of T cells with a CAR in as little as 24 hours in a more simplified manufacturing process without T cell activation or extensive culture outside the body also offers the possibility of expanding where and when these therapies are produced
https://www.pennmedicine.org/news/news-releases/2022/march/penn-researchers-shorten-manufacturing-time-for-car-t-cell-therapy
Longterm potential maybe? Good price to get in now? Could see how this could go up exponentially?
Donor T cells and donor genes to treat cancers?
Delivery of twin (AAV) capsids carrying 2 payloads: one with the nuclease to cut genomic DNA at the well-characterized PCSK9 locus and the other with a therapeutic donor gene, providing a potential path to permanent expression of a healthy gene
The long-term risks of off-target editing are unclear although
we are encouraged by the over 42 years of event free followup in 33 NHPs we have studied with this nuclease
I think you mentioned B2M going back. I know one group made a recombinant adenovirus carrying the gene and demonstrated recovery of HLA-I expression on cancer cells deficient in that. This lead to destruction by CD8+ T-cells https://onlinelibrary.wiley.com/doi/10.1111/j.1365-3083.2009.02276.x https://www.nature.com/articles/cgt201432
So that is one way. As for Tregs, ''In mice and humans, CCR8+ Tregs constituted 30 to 80% of tumor Tregs in various cancers and less than 10% of Tregs in other tissues, whereas most tumor-infiltrating conventional T cells (Tconvs) were CCR8–. CCR8+ tumor Tregs were highly differentiated and functionally stable.'' https://www.pnas.org/doi/10.1073/pnas.2114282119
The reason I mention that is due to a few anti-CCR8 mAbs in the clinic. So are anti-CD25 and anti-GARP mAbs https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7116816/ https://aacrjournals.org/cancerres/article/81/13_Supplement/1847/667728/Abstract-1847-Anti-GARP-antibody-DS-1055a-augments
I do think CAR-T's will have a role in treating solid tumours, but they will need to do more to overcome the hurdles that exist, such as immunosuppressive TMEs. I know they were working on shRNA to knockdown different genes, so expand that and look to incorporate a cassette to target a number.
Sounds like the second for up to five antigens. They haven't disclosed them or how Genentech identified the TCRs.
How about inserting MMR gene into MSI cancers and knock out gene expressing IL-1R1?
Hutch researchers scanned specimens representing 21 different cancer types. Looking only for the gene encoding the rarer IL-1R1 protein, they saw it pop up, at varying levels, among all 19 solid-tumor cancer types.
If DTIL can unsteath cancer cells before treating pts with stealth T cells from donors, ORR will be a lot higher. No need for neoantigens
ADXS called that HOT. It turned out to be ice as neoantigens are like fingerprints
It is ''personalised'' in a sense. ADAP will be responsible for developing clinical candidates using its iPSC platform, while Genentech responsible for the input of patient-specific neoantigen-reactive TCRs and subsequent clinical development and commercialisation.
Is 'personalized allogeneic' oxymoron?
I do think they should focus on their so-called stealth cells, so by the end of the year look to stop the PBCAR019 trial and focus on PBCAR019B. They also have another four targets https://www.businesswire.com/news/home/20210415005982/en/Precision-BioSciences-Reacquires-Global-Rights-to-its-Allogeneic-CAR-T-Programs
So make an assessment of them and maybe look to move PBCAR371A* into the clinic.
* An anti-CLL-1 CAR-T
I agree. RHHBY's Genentech signed a deal with ADAP https://www.globenewswire.com/news-release/2021/09/07/2292303/35803/en/Adaptimmune-Enters-into-a-Strategic-Collaboration-with-Genentech-to-Research-Develop-and-Commercialize-Cancer-targeted-Allogeneic-T-cell-Therapies.html
Both are iPSC-derived, but the most interesting is the personalised therapy (targeting neoantigens) they are working on together.
Cell therapy will be the backbone of therapies to treat solid tumors.
Roche is testing a mechanism that blocks TIGIT, a receptor capable of shrouding cancer cells from the immune system. Its drug, tiragolumab, binds to the receptor, preventing its deception. Roche added the new drug to its blockbuster medicine Tecentriq in patients with a form of lung cancer.
But during an interim analysis, Roche's regimen failed to meet the study's two key goals. It didn't have a statistically significant impact on the length of time before patients worsened — a measure known as progression-free survival. And it didn't improve overall survival.
https://www.investors.com/news/technology/biotech-stocks-arcus-and-others-hammered-on-roche-flop-in-lung-cancer/?src=A00220
NVS should buy DTIL with their stockpile of peanuts.
New YTB323 data https://library.ehaweb.org/eha/2022/eha2022-congress/357076/michael.dickinson.phase.i.study.of.ytb323.a.chimeric.antigen.receptor.28car29-t.html
Also, PHE885 https://library.ehaweb.org/eha/2022/eha2022-congress/358303/adam.s.sperling.phase.i.study.data.update.of.phe885.a.fully.human.html
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