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Rx Prescripttion Only-YMYL Medical Content
Adakras 200 mg Tablets (Adagrasib)
Adagrasib 200mg tablets – Everest Pharmaceuticals
Approved for adults with KRAS G12C-mutated locally advanced or metastatic non-small cell lung cancer (NSCLC) who have received at least one prior systemic therapy, and for KRAS G12C-mutated metastatic colorectal cancer (in combination with cetuximab) after prior fluoropyrimidine-, oxaliplatin-, and irinotecan-based chemotherapy.
- Clinical outcomes at a glance
43%
Objective response rate in previously treated NSCLC (KRYSTAL-1)
12.6 mo
Median overall survival in previously treated NSCLC (KRYSTAL-1)
6.5 mo
Median progression-free survival in NSCLC (KRYSTAL-1)
34%
Response rate in colorectal cancer with cetuximab (KRYSTAL-1 cohort)
- Am I a candidate? — Take Decesion
1
Confirm KRAS G12C mutation status
Requires tissue or liquid biopsy testing (NGS or PCR-based assay) showing the specific KRAS G12C mutation — other KRAS mutations (G12D, G12V, etc.) are not covered by this drug.
2
Identify your cancer type and treatment history
For NSCLC, used after at least one prior systemic therapy; for colorectal cancer, used with cetuximab after standard chemotherapy regimens have been tried.
3
Review liver function and cardiac (QTc) history with your oncologist
Baseline liver function tests and ECG are typically needed, especially if you take other medications that affect heart rhythm or are processed by the liver.
4
Discuss your goals of care
Weigh the response rate and survival data against GI side effects, twice-daily pill burden (multiple tablets per dose), and required liver/cardiac monitoring.
Important safety information: Adagrasib can cause liver problems (hepatotoxicity), which require liver function monitoring before and during treatment. It can also cause QTc prolongation (heart rhythm changes), interstitial lung disease (ILD)/pneumonitis, and significant gastrointestinal side effects including severe diarrhea, nausea, and vomiting. Tell your care team about all other medications you take, since adagrasib has notable drug interactions.
- common side effects to know
- Diarrhea (~63%)
- Nausea / vomiting (~60%)
- Fatigue
- Elevated liver enzymes
- Hepatotoxicity / liver injury
- QTc prolongation / ILD
- Trust & expertise
- FDA Approved 2022
- EMA Approved 2024
- NCCN NSCLC / CRC Guidelines
- KRYSTAL-1 / KRYSTAL-12
MD
Medical Oncologist Review
Board-certified oncologist · 12+ years in thoracic malignancies
“KRAS mutations were considered ‘undruggable’ for decades, so having an oral option for G12C-mutated lung and colorectal cancers is a significant shift. The GI side effects are common but usually manageable, and the drug interaction profile means a careful medication review at the start is essential — this isn’t a drug to start without going through your full medication list first.”
Content reviewed against FDA prescribing information, NCCN Guidelines v2.2024, and published Phase III trial data. Last updated June 2026.
Ready to discuss Tagrisso with your care team?
These steps help you have an informed conversation. A confirmed EGFR mutation result is the starting point for any treatment decision.
Questions to ask my healthcare provider
Before confirming adagrasib as your treatment
- Has my tumor been tested specifically for KRAS G12C — and is that confirmed, as opposed to a different KRAS mutation (like G12D or G12V) that wouldn’t respond to this drug?
- Was this testing done on tissue, blood, or both — and how recent is the sample?
- For my cancer type, is this being used as monotherapy (lung cancer) or in combination with cetuximab (colorectal cancer), and what does that combination look like practically?
- What treatments have I already had, and how does adagrasib fit into my overall treatment sequence?
About drug interactions — critically important for this drug
- Can we go through my complete medication list together, including over-the-counter drugs, supplements, and herbal products? Adagrasib has significant interactions.
- Are there specific medications I’m currently taking that will need to be adjusted, paused, or switched before I start?
- If I need a new medication prescribed by another doctor while on adagrasib, what should that doctor know — and should I have something in writing to share with them?
- Are there common over-the-counter products (like certain acid reflux medications) that I should avoid or use differently?
About liver and heart monitoring
- Will I need a baseline ECG, and how often will my heart rhythm be checked afterward?
- What symptoms — like dizziness, fainting, or a racing/irregular heartbeat — should prompt an urgent call?
- How often will my liver function be tested, and what would a concerning result mean for my treatment?
- What symptoms of liver problems (yellowing skin/eyes, dark urine, unusual fatigue, abdominal pain) should I watch for?
About the dosing schedule
- How many tablets do I take, and at what times — does the 600mg twice-daily dose mean three 200mg tablets each time?
- Does it matter if I take it with or without food?
- What should I do if I miss a dose, or if I vomit shortly after taking it (given how common nausea is)?
About managing GI side effects
- Given how common diarrhea and nausea are with this medication, should I have anti-diarrheal or anti-nausea medications on hand from day one?
- At what point would GI side effects be serious enough to need a dose adjustment or pause?
- Are there dietary changes that might help in the first few weeks?
About lung-related symptoms
- What are the early signs of pneumonitis or ILD (new or worsening cough, shortness of breath, fever) that I should report right away, rather than assuming it’s a cold?
About my specific situation
- How does my current liver and kidney function affect my starting dose?
- If I’m of childbearing potential, what precautions are needed during and after treatment?
About the longer road
- How will we track whether this is working — scan schedule and timing?
- If this stops working or side effects become unmanageable, what’s the next step? Is sotorasib (the other KRAS G12C inhibitor) an option at that point, or would it have similar limitations?
- Are there clinical trials worth knowing about, given how new this drug class is?
- Are there financial assistance programs through Bristol Myers Squibb if cost is a concern?
A practical tip: Because the drug interaction list is unusually long for this medication, it’s worth bringing a complete written list of everything you take — including supplements — to this appointment specifically, rather than relying on memory. Some interactions require timing adjustments rather than stopping a medication entirely, so your oncologist and pharmacist may need to work out a schedule together.
compare with other therapies
Both adagrasib and sotorasib are KRAS G12C inhibitors with overlapping indications, and — notably — neither has been tested directly against the other in a head-to-head trial. Here’s how they compare based on current data:
Approval timeline and indications
| Sotorasib (Lumakras) | Adagrasib (Adakras) | |
|---|---|---|
| Manufacturer | Amgen | Mirati Therapeutics / Bristol Myers Squibb |
| First approved | 2021 (NSCLC) | 2022 (NSCLC) |
| NSCLC indication | KRAS G12C-mutated NSCLC after ≥1 prior therapy | Same |
| CRC indication | In combination with panitumumab, for metastatic colorectal cancer with the KRAS G12C mutation, previously treated with fluoropyrimidine-, oxaliplatin-, and irinotecan-based chemotherapy | In combination with cetuximab, for KRAS G12C-mutated metastatic colorectal cancer with similar prior chemotherapy requirements |
| CRC approval type | First approval for chemorefractory KRAS G12C-mutated metastatic colorectal cancer,based on a phase III trial | First KRAS-targeting drug approved for colorectal cancer overall, via accelerated approval |
This is the most important update since our last conversation: both drugs now have FDA-approved colorectal cancer indications, each paired with a different EGFR-targeting antibody (panitumumab for sotorasib, cetuximab for adagrasib).
Dosing — a major day-to-day difference
| Sotorasib | Adagrasib | |
|---|---|---|
| Dose | 960mg once daily | 600mg twice daily |
| Pill burden | Typically 8 tablets (120mg each), once daily | Typically 3 tablets (200mg each) per dose, twice daily |
| Half-life | Shorter | Longer |
Sotorasib’s once-daily dosing means fewer total daily “events” but a high pill count at once; adagrasib’s twice-daily schedule spreads the pills out but means remembering doses morning and evening.
Efficacy in lung cancer
Both drugs showed broadly similar results in their pivotal NSCLC trials — response rates in the 37–43% range and progression-free survival in the 5–6.5 month range. Neither drug demonstrated an overall survival advantage over chemotherapy (docetaxel) in their respective phase III trials, which is an important honest point: these inhibitors as monotherapy in second-line treatment generally have relatively modest objective response rates and progression-free survival compared with other targeted therapies, and failed to demonstrate improvement in overall survival compared with docetaxel in phase III studies, largely due to resistance developing over time.
Efficacy in colorectal cancer — both drugs underperform here
This is a critical point for anyone with KRAS G12C-mutated CRC specifically: while both sotorasib and adagrasib showed efficacy in NSCLC, they were considerably less effective for colorectal cancer patients with the same mutation, which is why both are approved only in combination with an EGFR-blocking antibody for CRC, never as monotherapy.
For sotorasib + panitumumab (CodeBreaK 300), 26% of patients treated with the approved 960mg dose experienced a treatment response, compared with 0% on standard-of-care — a meaningful improvement over nothing, but still a modest absolute response rate.
For adagrasib + cetuximab, direct trial-by-trial efficacy figures are available from KRYSTAL-1, though as research reviewers note, we currently do not have clinical trials or real-world data directly comparing the efficacy of adagrasib to sotorasib in this setting, and any cross-trial comparison suggesting one numerically outperforms the other should be read cautiously given the differences in trial design.
A phase III trial (KRYSTAL-10) comparing adagrasib plus cetuximab against standard chemotherapy in second-line KRAS G12C-mutated colorectal cancer is underway, with results expected in 2026 — so the evidence picture for adagrasib in CRC is still maturing relative to sotorasib’s completed phase III data.
Why both underperform in CRC
The shared explanation across both drugs comes down to EGFR pathway feedback — when KRAS G12C is blocked, colorectal cancer cells can reactivate growth signals through EGFR, essentially routing around the blockade. This is why combined KRAS G12C and EGFR inhibition — whether sotorasib-panitumumab, adagrasib-cetuximab, or other combinations in development — has shown greater efficacy than KRAS G12C inhibitor monotherapy, and supports this combination approach as the standard regimen for this population.
Side effect profiles
Both drugs share a broadly similar adverse event pattern — GI toxicity (diarrhea, nausea), hepatotoxicity requiring liver monitoring, and some cardiac (QT-related) considerations. Adagrasib’s longer half-life and more complex drug-metabolism interactions (which we discussed earlier) are generally considered more pronounced than sotorasib’s, making the medication review conversation particularly important if adagrasib is being considered.
Where CRC patients now stand vs. before
Before these approvals, options for KRAS G12C-mutated CRC after standard chemo were limited to non-targeted late-line therapies — prior to this approval, standards of care included trifluridine/tipiracil and regorafenib, which yielded positive but limited survival outcomes — drugs we discussed earlier in this conversation. Both new combinations represent a step forward, though the absolute benefit (around a quarter of patients responding) means expectations should be calibrated honestly.
Bottom line
For NSCLC, the two drugs are largely interchangeable in efficacy, with the choice often coming down to dosing preference (once-daily/high pill count vs. twice-daily) and drug interaction considerations. For CRC, both are now viable — sotorasib+panitumumab has completed phase III data supporting its approval, while adagrasib+cetuximab’s confirmatory phase III data (KRYSTAL-10) is still pending results expected in 2026. Your oncologist’s experience with each combination, your specific medication list (given adagrasib’s interaction profile), and which EGFR-antibody partner (cetuximab vs panitumumab) your treatment center is set up to administer may all factor into which combination is recommended.
How does testing work
KRAS G12C testing follows the same general logic as the EGFR, FLT3, BCR-ABL, and PIK3CA/AKT1/PTEN testing we’ve discussed — but KRAS testing has one notable historical wrinkle: for decades, KRAS mutations were tested mainly to exclude patients from EGFR-targeted therapies (since KRAS-mutant tumors don’t respond to EGFR inhibitors), not to select them for a KRAS-targeted drug. That changed only recently with adagrasib and sotorasib.
What’s being tested
KRAS G12C is a single, specific point mutation — a substitution at codon 12 of the KRAS gene where glycine is replaced by cysteine. This is just one of many possible KRAS mutations (others include G12D, G12V, G13D, and more), and only G12C is targetable by adagrasib or sotorasib. The other KRAS mutations remain largely untargeted by approved drugs, though some are in earlier-stage development (as we touched on with the KRAS-G12D inhibitor mentioned in research).
This specificity is important: a tumor that’s broadly “KRAS-mutant” doesn’t qualify for these drugs — it has to be the G12C variant specifically.
Sample source
Both tissue and blood-based testing are used:
Tumor tissue — from a biopsy or surgical specimen, either archival or fresh, is the traditional source and allows broad genomic profiling alongside other relevant markers (PD-L1, other co-mutations like STK11 or KEAP1 that affect prognosis).
Liquid biopsy (blood-based ctDNA) — increasingly used, especially when tissue is limited or a fresh biopsy isn’t practical. This was validated as part of the companion diagnostic pathways for both adagrasib and sotorasib.
How the lab analyzes it
- Next-generation sequencing (NGS) panels — the most common approach now, since most lung and colorectal cancer patients already get broad NGS panels at diagnosis (covering EGFR, ALK, ROS1, KRAS, and many other genes simultaneously). KRAS G12C is typically just one result within a larger panel report.
- PCR-based companion diagnostics — specific FDA-approved tests (such as the therascreen KRAS RGQ PCR Kit) were validated alongside the drug approvals and remain in use, particularly for tissue-based testing in some labs.
- Liquid biopsy NGS assays — validated companion diagnostics also exist for blood-based detection.
Timeline
Similar to other NGS-based testing: tissue-based comprehensive panels typically take 1–3 weeks, while liquid biopsy results often return in 1–2 weeks. Since KRAS testing is usually bundled into a broad genomic panel done at diagnosis (rather than ordered as a standalone test later), many patients already have this information available by the time treatment decisions are being made — unlike, say, T790M testing in EGFR-mutated lung cancer, which is specifically triggered by disease progression.
What the result means for treatment
| Result | What it typically means |
|---|---|
| KRAS G12C detected | Adagrasib or sotorasib become potential options (NSCLC monotherapy, or combination therapy for CRC) |
| KRAS mutation detected, but not G12C (e.g., G12D, G12V) | Neither approved KRAS G12C inhibitor applies; other treatment lines considered, though clinical trials for other KRAS variants are an active research area |
| KRAS wild-type (no mutation) | KRAS-targeted therapy not relevant; other biomarkers (EGFR, ALK, PD-L1, etc.) guide treatment |
A practical nuance
Because KRAS testing is usually part of a broad upfront panel rather than a separately-ordered test, it’s worth specifically checking your original pathology or molecular report for the exact KRAS mutation listed — not just “KRAS mutation positive” or “KRAS mutation negative.” If the report says something general without specifying G12C versus another variant, that’s worth clarifying with your oncologist, since it directly determines whether adagrasib or sotorasib are even on the table.
Medical disclaimer: This page is for informational purposes only and does not constitute medical advice, diagnosis, or treatment. Osimertinib is a prescription medication that must only be used under the supervision of a qualified oncologist. Clinical outcomes data is drawn from published Phase III trials; individual results vary. Always consult your healthcare provider and refer to the full prescribing information before making any treatment decisions. Emergency: call your local emergency services or poison control immediately if you experience serious adverse effects.
