Scientist interested in films, music, photography, art and nature but my biggest passion is #Science
Joined June 2009
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Jorge Benitez retweeted
Rezatapopt (PC14586) is an oral, first-in-class small-molecule p53 reactivator currently being evaluated in the PYNNACLE clinical trial (NCT04585750) for patients with locally advanced or metastatic solid tumors carrying a specific TP53 Y220C mutation.
The development of KRAS inhibitors has ushered in a new wave of research on therapeutic targeting of mutant p53. Learn more about these approaches on the #AACRBlog: brnw.ch/21x70lN @kevansf @UCSF
Jorge Benitez retweeted
At #ESMO26 we introduced a new word, #RIPTAC, JNJ-6143. Introducing another innovation presented @sitcancer yesterday! FIH Investigational combo of Pasritamig our @JNJInnovMed KLK2xCD3 T-cell agent + our PSMA x CD28 co-stim JNJ-9401. Signal 1 & signal 2 together! #MyCompany
Jorge Benitez retweeted
Try this. There are no “subtypes.” Each individual patient is different and can be defined at the molecular level by technology that is now routinely available in many countries.
Hallmarks of colorectal cancer subtypes👇
nature.com/articles/s41568-0…
(Origins and heterogeneity of colorectal cancer)
Jorge Benitez retweeted
Beautiful illustration of our work -- Cover art @CellStemCell
📄 Paper link: lnkd.in/eCjhgxW7
"Subtractive engineering" for #morphogenesis #organoids #SCEM #embryoids
👀 for more info : teapawt.net/MoEbrahimkhani/status/…
1/10 What if building tissues requires not only adding the right cells, materials or ECMs, but removing the wrong ones too? (free link at 10/10)
#Development builds through both construction and elimination. Yet tissue engineering largely focuses on addition. We do not have a #subtractive framework in our synthetic in. whereas tissues operate far from the constraints exist in vivo.
Our new @CellStemCell paper explores the missing half: "Subtractive Tissue Engineering" is how we named it. #development #celldeath #syntheticbiology #systemsbiology #embryogenesis #organoids #NAMs #human #stemcells🧵
ALT Programmable subtraction for tissue engineering
Jorge Benitez retweeted
The Ivy Brain Tumor Center is conducting a new Phase 0/2 study evaluating the investigational drug BGB-58067 for newly diagnosed GBM patients.
Learn more: bar.rw/3W7C6IR
602-406-8605
Jorge Benitez retweeted
Check out Georg Nagel – the 2026 medicine prize laureate – wearing a blue helmet and a big smile, cycling into the University of Würzburg to a warm welcome full of balloons and applause from students.
Check out his first reaction interview here: bit.ly/4yO0fBH
Discovery and Characterization of Divarasib (GDC-6036), a Potent Covalent Inhibitor of KRAS G12C | Journal of Medicinal Chemistry | ACS Publications pubs.acs.org/jmcmar/article/…
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Jorge Benitez retweeted
JNJ-6143, first-in-class oral AR-BRD4 RIPTAC, phase 1 mCRPC: a wide window between efficacy and safety. n=105, doses 12.5 to 150 mg.
📈 50 mg daily: PSA50 77%, PSA90 48%, confirmed ORR 69%, after a median 4 prior lines
📊 PSA declines seen from 12.5 to 150 mg. 66% of all patients still on drug
🔍 At 50 mg: 58% any-grade TRAEs, no serious TRAEs. Median DOR 11.0 months, CI 5.9 to NE
Activity across a 12-fold dose range. Phase 2 is open at 50 mg.
Congrats to @BGarmezy on the presentation and all the investigators.
#ESMO26 #ProstateCancer #mCRPC #GUonc
Jorge Benitez retweeted
What can we learn from all cytokines in the human genome? For most, we have limited info on what they do and when to target them
Meet TAPAS & EPICURE: tools to synthesize all human cytokines➡️scRNA data of primary human immune responses➡️🖥️methods to use them in your work (1/n)
Divarasib as Compared with Sotorasib or Adagrasib in KRAS G12C–Mutated NSCLC | New England Journal of Medicine nejm.org/doi/full/10.1056/NE…
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Jorge Benitez retweeted
#ESMO26 Dr. @tnewsomdavis shows some of the clinical data of bispecifics, trispecifics, and T-cell engagers. Why bispecifics targeting PD(L)1 and VEGF can be upgrades. Why T-cell engagers can disrupt cancers in unique ways. #ESMOAmbassadors
Jorge Benitez retweeted
1/3
It's understandable why oncologists and patients want crossover, and it's easy to argue for it after a positive trial. But when the trial was designed, no one knew divarasib would win, and G12Ci after G12Ci was unproven. Crossover makes sense when the later-line benefit is already established.
“If PFS is the primary endpoint, why isn't crossover allowed?”
I haven't heard a more justified complaint from an oncologist in a long time.
Dr. Benjamin Besse💯👏👏
#ESMO26
Jorge Benitez retweeted
GFH276 pan-RAS (ON) molecular glue
➡️ph1/1b data; n=73 PDAC ,5-320mg
➡️no . prior lines tx =2
➡️ORR 41% in #PDAC, @ 40-160mg,
small nos with prior RASi
➡️Rash most common AE
As many trials move quickly to 1st line, how will we sequence??
@myESMO #ESMO26 @OncoAlert
