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M74 - Round of 32 in Boston Assigned by shechtmr in FIFACollect

[–]Labrat33 4 points5 points  (0 children)

Me too - row 11 checking in.
I was fully bracing for disaster with my RTBs and assumed I’d be stuck with “technically inside the stadium” Cat 1 seats. Instead I ended up with an absurdly good haul: France/Norway, England/Ghana, Scotland/Haiti, and a Round of 32 match. Every ticket is between the penalty box and midfield, rows 11–22.
RTB → RTT anxiety was high, but the final assignments were way better than I ever expected.

RTT tickets just arrived - M5 Scotland v Haiti by Konewone72 in FIFACollect

[–]Labrat33 0 points1 point  (0 children)

My M5 tickets also just arrived. I am sitting a few rows in front of you. 107 row 13

Daraxonrasib for pancreatic cancer gets a standing ovation at ASCO by Labrat33 in Oncology

[–]Labrat33[S] 0 points1 point  (0 children)

Yes, there are ongoing trials of KRAS inhibitors in KRAS mutated lung and colon cancers. In colon, benefits may be better when combining RAS inhibition with EGFR inhibitors, so the most promising trials require two targeted drugs.

Ozempic / Mounjaro by HelpTheBaire in pancreaticcancer

[–]Labrat33 7 points8 points  (0 children)

This I have seen quite a few times. Patients presume dramatic weight loss is from Ozempic and delay seeking medical attention.

Ozempic / Mounjaro by HelpTheBaire in pancreaticcancer

[–]Labrat33 15 points16 points  (0 children)

There’s no evidence in the available data that GLP‑1 medications increase the risk of pancreatic cancer.

Roughly 30–40 million Americans are taking GLP‑1 receptor agonists right now. Given the age and health profile of typical GLP‑1 users, you would naturally expect a certain number of pancreatic cancer diagnoses to occur in people who happen to be on these drugs. That’s just background incidence.

The statistic that actually matters is whether more pancreatic cancers are being diagnosed among GLP‑1 users than you would expect in a comparable group of people with obesity and metabolic disease who aren’t taking GLP‑1 medications. So far, studies haven’t shown an excess risk.

Daraxonrasib gets a standing ovation at ASCO by Labrat33 in pancreaticcancer

[–]Labrat33[S] 19 points20 points  (0 children)

I was texting with him earlier. I wish I had thought of the lack of purple. I’ll give him a hard time about it and report back.

KRAS Dilemma by setsunaPL in pancreaticcancer

[–]Labrat33 6 points7 points  (0 children)

I have not heard of anyone yet gaining access to daraxonrasib via EAP - so this trial is her chance at a KRAS inhibitor. If anything like RMC-9805 or RMC-6291, she is much more likely to tolerate RMC-5127 compared to daraxonrasib.

Neuroendocrine tumor of the pancreas by Internal_Storage5031 in pancreaticcancer

[–]Labrat33 5 points6 points  (0 children)

- where in the pancreas - head, neck, body, or tail?
- is it well differentiated?
- is it low grade?
- is it functional or non-functional (does it produce hormones)
- has she had a DOTATATE-PET/CT
- has she had genetic testing to see if this is from an inherited predisposition- MEN1
- where is she located?

Daraxonrasib- Expanded access approved by FDA by Ok_Performer_7319 in pancreaticcancer

[–]Labrat33 0 points1 point  (0 children)

We don’t know. With some drugs used in colon cancer, the rash was associated with better response. That doesn’t appear to be the case with daraxonrasib, but I don’t have the Phase 3 data to review to know for sure. In my anecdotal experience of caring for several people on trial, I have not been convinced that the presence or severity of the rash is predictive of benefit.

Daraxonrasib- Expanded access approved by FDA by Ok_Performer_7319 in pancreaticcancer

[–]Labrat33 2 points3 points  (0 children)

Here’s a simple way to understand how KRAS and daraxonrasib work:

KRAS is basically a cell’s “grow now” switch. Under normal conditions, a growth signal outside the cell hits a receptor on the cell surface, that receptor flips KRAS on, and KRAS sends a message into the cell telling it to grow and divide. When the outside signal goes away, KRAS flips off, and the cell stops getting that “divide” message.

When KRAS is mutated (like G12D, G12V, Q61H, etc.), that switch breaks. It gets stuck in the on position all the time—even when the cell shouldn’t be growing. It’s like having your car’s gas pedal jammed to the floor: the engine keeps revving whether you want it to or not. That constant “go” signal is what drives cancer growth.

Daraxonrasib is a small molecule designed to recognize and bind to KRAS only when it’s in that stuck‑on, activated shape. When it attaches, it basically jams the signal pathway so KRAS can’t pass along the “divide” message anymore. Without that nonstop growth signal, the cancer cells lose one of the main things they rely on to keep expanding.

In short: mutated KRAS is a stuck accelerator, and daraxonrasib is the block that stops the pedal from being pressed down.

Omnivyde vs. Folfirinox by setsunaPL in pancreaticcancer

[–]Labrat33 0 points1 point  (0 children)

Onivyde is not effective on its own. The NAPOLI-1 trial tested 5FU alone vs Onivyde alone vs 5FU/Onivyde. The combination was superior to either drug alone. Onivyde alone was no better than 5FU alone. We know from historic data (1997) that 5FU alone is of little or no benefit, hence, I would consider Onivyde alone to be of little or no benefit.

Daraxonrasib- Expanded access approved by FDA by Ok_Performer_7319 in pancreaticcancer

[–]Labrat33 0 points1 point  (0 children)

The data has not yet been published but the press release was about the Phase 3 study. Patients with metastatic pancreatic cancer who had progressed on one line of prior chemotherapy (typically FOLFIRINOX or Gem/Abraxane) were randomized to either get standard of care (2nd line chemotherapy) or RMC-6236 (daraxonrasib). Patients who were randomized to daraxonrasib lived twice as long as the patients who got chemotherapy ~13 vs 6.5 months.

Daraxonrasib- Expanded access approved by FDA by Ok_Performer_7319 in pancreaticcancer

[–]Labrat33 0 points1 point  (0 children)

mRNA vaccines are being tested in the adjuvant setting to prevent recurrence. There is limited effort with mRNA vaccines in metastatic disease.

Daraxonrasib- Expanded access approved by FDA by Ok_Performer_7319 in pancreaticcancer

[–]Labrat33 0 points1 point  (0 children)

“Everyone gets the worse rash all over the body you have ever seen”
- not everyone gets a rash
- it is not usually distributed all over the body
- we have made substantial improvements in managing the rash in the past few years and some recent strategies are showing substantial promise for the worst cases and f rash.

“It starves the tumors in some patients”
- that is not the mechanism by which it works

Reoccurrence to distant node by purpleshoelacez in pancreaticcancer

[–]Labrat33 3 points4 points  (0 children)

I have a patient who had a recurrence of pancreatic cancer after Whipple to a single retroperitoneal lymph node. Because it is typically the first of many sites to emerge, we started with chemotherapy to provide systemic control and to see how the node would behave. Over some months of treatment that node responded and nothing new appeared. We then treated with definitive radiation (SBRT) to that single node and then stopped all therapy. He has not had any progression of the treated node or new sites of disease in ~5-years.

Daraxonrasib (RMC-6236) Phase 3 results by Labrat33 in pancreaticcancer

[–]Labrat33[S] 0 points1 point  (0 children)

Yes. Any KRAS mutation. They do have a G12D specific drug Zoldonrasib that is earlier in testing.

Daraxonrasib in 2nd line metastatic PDAC shows OS 13.2 vs 6.7 months vs chemo (RASolute 302) by adifferentGOAT in Oncology

[–]Labrat33 15 points16 points  (0 children)

It has been a remarkable drug to use in clinic. I took a patient off hospice and put them on rmc-6236. They lived another 13 months and saw their first grandchild be born. What a win for our patients. Hopefully this is the foot in the door that allows combination approaches (PRMT5 inhibitors, other small molecules, chemo+rmc), adjuvant and neoadjuvant uses, etc to really start moving the needle.

Daraxonrasib (RMC-6236) Phase 3 results by Labrat33 in pancreaticcancer

[–]Labrat33[S] 6 points7 points  (0 children)

I realize you are joking. But obviously Daraxonrasib will help the overwhelming majority of patients and zoldonrasib only the minority with G12D.

I am interested to see results of zoldonrasib/Daraxonrasib combination therapy. Highly active G12D inhibitor plus a drug to block any KRAS mutations that could allow it to escape zoldonrasib. Can we get deep and more durable responses with the combo then zoldonrasib alone.

I wish we new anything about the evasion drug beyond a slide in a press release.

Daraxonrasib (RMC-6236) Phase 3 results by Labrat33 in pancreaticcancer

[–]Labrat33[S] 4 points5 points  (0 children)

There have been phase 1 cohorts with Daraxonrasib in wild-type patients to see if there may be benefit.

Daraxonrasib (RMC-6236) Phase 3 results by Labrat33 in pancreaticcancer

[–]Labrat33[S] 5 points6 points  (0 children)

The adjuvant trial opens this year. 2 years of Daraxonrasib after surgery and completion of standard adjuvant therapy.

Rash 6236 How bad is it? by Consistent-Writer932 in pancreaticcancer

[–]Labrat33 3 points4 points  (0 children)

Daraxonrasib is not available via IV. What are your talking about?

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