The Current State of the Art in KRAS G12C Mutation: From Sotorasib to Divarasib and ESMO 2026
In this article
From the "Undruggable" Gene to Personalized Treatment: 40 Years of KRAS G12C Targeted Therapy and ESMO 2026
KRAS is one of the most frequently altered genes in cancer, and for decades it was described as "undruggable." The approval of sotorasib in 2021 overturned that belief, but the effect of first-generation KRAS G12C inhibitors turned out to be more limited than hoped. The Krascendo 1 trial, presented at the ESMO 2026 Presidential Symposium and published in the New England Journal of Medicine, is the first head-to-head comparison to show that the second-generation drug divarasib prolongs survival compared with first-generation drugs. In this review, we cover the history of KRAS G12C targeted therapies, their results in lung, colorectal and pancreatic cancer, direct and indirect comparisons, and the situation in Turkey. We have covered the results in EGFR-mutated lung cancer and PD-L1-negative lung cancer presented at the same congress, our ESMO 2026 preview and WCLC 2026 in separate articles.
- Who has it: The KRAS G12C mutation is found in about 13% of lung adenocarcinomas (mostly in people who have smoked), 3–4% of colorectal cancers and 1–2% of pancreatic cancers.
- Lung cancer, second line: Sotorasib (2021) and adagrasib (2022) are approved. Compared with docetaxel, they modestly prolonged progression-free survival (5.6 vs 4.5 months and 5.5 vs 3.8 months), but no overall survival benefit was shown.
- ESMO 2026 · Krascendo 1: Compared with sotorasib or adagrasib, divarasib prolonged progression-free survival (9.8 vs 5.7 months; HR 0.58) and overall survival (17.7 vs 12.0 months; HR 0.56), with fewer serious adverse events. It is not yet approved.
- Colorectal and pancreatic cancer: In colorectal cancer, a KRAS G12C inhibitor is given together with an EGFR antibody; however, the approval of adagrasib + cetuximab was withdrawn in September 2026 after the confirmatory trial failed. In pancreatic cancer, response rates are around 20–35%.
- Turkey: Sotorasib is licensed; adagrasib is not. Access to new drugs such as divarasib and olomorasib is possible only through clinical trials.
Why does this matter?
RAS genes (KRAS, NRAS, HRAS) are mutated in about a quarter of human cancers. The KRAS protein works like an "on/off switch" that regulates cell growth. A mutation causes the switch to stay in the on position, so the cell receives a constant growth signal. Because the surface of the KRAS protein is smooth and has no obvious pocket for drugs to bind to, for many years no drug could be developed against it.
There are different subtypes of KRAS mutations, such as G12C, G12D, G12V and G13D. In the G12C mutation, the glycine at position 12 of the protein is replaced by cysteine. This cysteine provided an anchor point to which drugs can bind permanently (covalently), and the first successful KRAS drugs were developed for this subtype. In lung cancer, the KRAS G12C mutation is associated with smoking, and some patients also have co-mutations such as STK11 or KEAP1 that adversely affect the response to treatment (the link between smoking and cancer). Comprehensive molecular testing at diagnosis is essential for treatment decisions (next-generation sequencing).
Figure 1 · How does KRAS work, and where do the drugs bind?
Simplified diagram
Which treatments are used today in KRAS G12C-mutated lung cancer?
In the first line, standard treatment is immunotherapy or chemotherapy + immunotherapy, depending on the PD-L1 level. When the disease progresses after this treatment, sotorasib or adagrasib can be used; both modestly prolonged progression-free survival compared with docetaxel. At ESMO 2026, divarasib prolonged survival compared with these two drugs. Moving KRAS G12C inhibitors into the first line is being investigated in phase 3 trials.
Lung cancer: what did the first-generation drugs achieve?
Sotorasib and adagrasib were first approved on the basis of single-arm phase 1/2 trials in patients who had previously received chemotherapy and immunotherapy. Both were then tested against docetaxel in randomized phase 3 trials.
| Trial | Treatment | Patients | Response rate | Median progression-free survival | Median overall survival |
|---|---|---|---|---|---|
| CodeBreaK 100 (phase 2, 2021) | Sotorasib | 126 | 37.1% | 6.8 months | 12.5 months |
| KRYSTAL-1 (phase 2, 2022) | Adagrasib | 116 | 42.9% | 6.5 months | 12.6 months |
| CodeBreaK 200 (phase 3, 2022) | Sotorasib / docetaxel | 345 | 28.1% / 13.2% | 5.6 / 4.5 months (HR 0.66) | 10.6 / 11.3 months (no difference) |
| KRYSTAL-12 (phase 3, 2024–2025) | Adagrasib / docetaxel | 453 | 32% / 9% | 5.5 / 3.8 months (HR 0.58) | Not yet mature |
A hazard ratio (HR) below 1 favors the experimental arm. In CodeBreaK 200, some patients in the docetaxel arm crossed over to sotorasib after progression; this may be one of the reasons why no overall survival difference was seen.
Response rate in previously treated lung cancer
Objective response rate in single-arm trials (%).
Values for divarasib, fulzerasib and glecirasib come from early-phase or single-arm registration trials. Comparisons across different studies are indirect; patient populations, prior treatments and follow-up differ.
Phase 3: first-generation drugs vs docetaxel
Median progression-free survival (months). Experimental arm in color, docetaxel arm in gray.
CodeBreaK 200: HR 0.66; KRYSTAL-12: HR 0.58. In CodeBreaK 200, no overall survival difference was seen (10.6 vs 11.3 months). Comparisons across different studies are indirect; patient populations, prior treatments and follow-up differ.
These results showed two things: KRAS G12C inhibitors are more effective than docetaxel and can be taken as tablets, but their effect falls far short of the long-lasting control achieved with EGFR or ALK inhibitors. Median progression-free survival remained around 6 months. In December 2023, the FDA declined to grant sotorasib full approval on the grounds that the progression-free survival data from CodeBreaK 200 could not be reliably interpreted, and requested a new confirmatory trial to be completed by 2028; the accelerated approval remains in place. During this process, the standard dose of sotorasib was set at 960 mg.
Side effects
The main side effects of the first-generation drugs are diarrhea, nausea, fatigue and elevated liver enzymes. Liver toxicity can be more frequent and more severe, especially in patients who start sotorasib shortly after immunotherapy; liver tests are therefore closely monitored during the first months of treatment. With adagrasib, heart rhythm (QT prolongation) also needs to be monitored. Adagrasib has also been shown to be active against brain metastases; in KRYSTAL-12, the intracranial response rate in patients with brain metastases was 24% vs 11%.
Real-world data from Turkey
In a Turkish Oncology Group study of 41 patients from 15 centers, sotorasib achieved a response rate of 34.2%, a median progression-free survival of 8.3 months and a median overall survival of 15.8 months; the rate of grade 3–4 adverse events was 12.2%. These results are consistent with international trials.
KRAS G12C inhibitors approved in China
In 2024–2025, three new KRAS G12C inhibitors received conditional approval in China for previously treated lung cancer. Response rates in single-arm trials are around 50%; however, these drugs have not been compared head-to-head with first-generation drugs and are not approved outside China.
- Fulzerasib (2024): China's first KRAS G12C inhibitor. Response rate 49.1%, median progression-free survival 9.7 months.
- Garsorasib (2024–2025): Conditional approval for patients who have received at least one systemic therapy.
- Glecirasib (May 2025): Response rate 49.6%, median progression-free survival 8.2 months, median overall survival 17.5 months.
ESMO 2026: the second-generation era begins with Krascendo 1
Divarasib (Roche) is a second-generation KRAS G12C inhibitor that was found in laboratory studies to be 5–20 times more potent and more selective than sotorasib and adagrasib. In the phase 1 study in lung cancer, the response rate was 53.4% and median progression-free survival was 13.1 months. Krascendo 1 is the first phase 3 trial to compare a KRAS G12C inhibitor head-to-head with approved KRAS G12C inhibitors.
Figure 2 · Design of the Krascendo 1 trial
Open-label, randomized, global phase 3 trial (26 countries, 151 centers)
| Outcome | Divarasib (167 patients) | Sotorasib or adagrasib (171 patients) | Difference |
|---|---|---|---|
| Median progression-free survival (independent review) | 9.8 months | 5.7 months | HR 0.58 (95% CI 0.44–0.76); p<0.0001 |
| Proportion of patients progression-free at 12 months | 43.9% | 24.0% | About 20 points |
| Median overall survival | 17.7 months | 12.0 months | HR 0.56 (95% CI 0.41–0.78); p=0.0005 |
| Proportion of patients alive at 12 months | 67.1% | 49.2% | About 18 points |
| Confirmed response rate | 58.4% | 32.3% | About 26 points |
| Median duration of response | 11.9 months | 6.9 months | – |
| Grade 3 or higher treatment-related adverse events | 24.6% | 34.5% | Fewer with divarasib |
| Treatment discontinuation due to adverse events | 4.8% | 11.7% | Fewer with divarasib |
| Median duration of treatment | 11.3 months | 5.0 months | – |
In the control arm, 156 patients received sotorasib and 15 received adagrasib. Median follow-up was 14.3 months. CI: confidence interval. No treatment-related loss of life occurred in either arm.
Krascendo 1: divarasib vs first-generation drugs
Median progression-free and overall survival (months). Colored bar divarasib, gray bar sotorasib or adagrasib.
Progression-free survival HR 0.58 (p<0.0001); overall survival HR 0.56 (p=0.0005). Median follow-up 14.3 months.
Figure 3 · In Krascendo 1, how many of every 100 patients were alive at 12 months?
Rounded values (67.1% and 49.2%)
Krascendo 1: response and side effects
Proportion of patients (%). Colored bar divarasib, gray bar sotorasib or adagrasib; red bar side effects.
Median duration of use was 11.3 months for divarasib and 5.0 months for the control drugs.
What stands out is that divarasib was both more effective and better tolerated: although patients took divarasib for about twice as long, serious adverse events and treatment discontinuation were less frequent. As expected for this drug class, the most common side effects were gastrointestinal side effects and elevated liver enzymes. Limitations of the trial: the open-label design, the small number of patients receiving adagrasib in the control arm, and the exclusion of patients with untreated brain metastases.
Can they move into the first line?
KRAS G12C-mutated lung cancer can progress rapidly, and a substantial proportion of patients never reach second-line treatment. For this reason, the use of KRAS G12C inhibitors in the first line together with immunotherapy and/or chemotherapy is being investigated. Early results are promising; however, no phase 3 trial has reported results yet, and immunotherapy-based treatment remains the standard in the first line (proper planning of immunotherapy).
| Trial (phase) | Treatment | Patient group | Response rate | Progression-free survival |
|---|---|---|---|---|
| KRYSTAL-7 (phase 2) | Adagrasib + pembrolizumab | PD-L1 50% or higher (54 patients) | 59.3% | Median 27.7 months |
| CodeBreaK 101 (phase 1b) | Sotorasib + carboplatin-pemetrexed | First line (37 patients) | 65% | Median 10.8 months |
| Olomorasib (phase 1/2 · ESMO 2026) | Olomorasib + pembrolizumab + chemotherapy | First line (77 patients) | 62% | Median 11.6 months |
| Olomorasib (phase 1/2 · ESMO 2026) | Olomorasib + pembrolizumab | First line (85 patients; 64% with PD-L1 50% or higher) | Not reported | 55% progression-free at 18 months |
| Krascendo 170 (phase 1b/2 · ASCO 2026) | Divarasib + pembrolizumab | Advanced disease | 69.6% (unconfirmed) | Not reported |
These are single-arm trials and cannot be compared with one another. Liver side effects may increase when a KRAS G12C inhibitor is given together with immunotherapy; in KRYSTAL-7, the rate of grade 3–4 treatment-related adverse events across all patients was 68.4%.
Early results in the first line
Objective response rate in single-arm trials (%).
Patient populations, PD-L1 distribution and response assessment methods differ. Comparisons across different studies are indirect; patient populations, prior treatments and follow-up differ.
- KRYSTAL-7: Adagrasib + pembrolizumab vs pembrolizumab alone (PD-L1 50% or higher).
- CodeBreaK 202: Sotorasib + carboplatin-pemetrexed vs pembrolizumab + carboplatin-pemetrexed (PD-L1-negative; about 750 patients).
- SUNRAY-01: Olomorasib + pembrolizumab (PD-L1 50% or higher) or olomorasib + chemoimmunotherapy vs placebo; first results are expected in the first half of 2027.
- Krascendo 2: Divarasib + pembrolizumab vs chemoimmunotherapy.
Colorectal cancer: why is a single drug not enough?
In colorectal cancer, KRAS G12C inhibitors given alone achieve low response rates (about 10% with sotorasib and around 20% with adagrasib). This is because, when KRAS is blocked, tumor cells reopen the signaling pathway through EGFR. For this reason, in colorectal cancer KRAS G12C inhibitors are given together with EGFR antibodies (panitumumab or cetuximab) (treatment of colon and rectal cancer).
| Trial | Treatment / control | Response rate | Progression-free survival | Overall survival | Status |
|---|---|---|---|---|---|
| CodeBreaK 300 (phase 3) | Sotorasib 960 mg + panitumumab / trifluridine-tipiracil or regorafenib | 30.2% / 1.9% | 5.6 / 2.2 months | HR 0.70 (not significant) | FDA approval January 2025 |
| KRYSTAL-1 (phase 2) | Adagrasib + cetuximab | 34–43% | About 7 months | – | FDA accelerated approval June 2024 |
| KRYSTAL-10 (phase 3) | Adagrasib + cetuximab / FOLFIRI or mFOLFOX6 (second line) | 47% / 16% | 7.5 / 8.1 months | 21.6 / 21.7 months | Approval withdrawn in September 2026 |
CodeBreaK 300 was conducted in chemotherapy-refractory patients and KRYSTAL-10 in the second line; because the control arms differ, the results cannot be compared directly.
Phase 3 trials in colorectal cancer
Median progression-free survival (months). Experimental arm in color, control arm in gray.
CodeBreaK 300 was conducted in chemotherapy-refractory patients and KRYSTAL-10 in the second line. In KRYSTAL-10 the difference was not significant and the approval was withdrawn. Comparisons across different studies are indirect; patient populations, prior treatments and follow-up differ.
KRYSTAL-10 is an important example showing that a higher response rate does not always mean longer survival: with adagrasib + cetuximab, tumor shrinkage was three times more frequent, yet progression-free and overall survival were the same as with second-line chemotherapy. In colorectal cancer, KRAS G12C targeted therapy is today an option for chemotherapy-refractory patients; its use together with chemotherapy in the first line is being investigated (Lonsurf + bevacizumab in chemotherapy-refractory colorectal cancer, FOLFIRI + bevacizumab).
Pancreatic cancer and other tumors
More than 90% of pancreatic cancers carry a KRAS mutation, but only 1–2% of these are of the G12C type; the most common type is G12D. In previously treated KRAS G12C-mutated pancreatic cancer, response rates of 21% with sotorasib and about 33% with adagrasib have been reported. Olomorasib received Breakthrough Therapy designation from the FDA in this group. The real hope, however, lies in pan-RAS drugs that target all RAS mutations: daraxonrasib is being tested in a phase 3 trial in pancreatic cancer (daraxonrasib and resistance, recent advances in pancreatic cancer). The KRAS G12C mutation can also occur in rarer tumors such as biliary tract, small intestine, appendix and ovarian cancers; responses to KRAS G12C inhibitors have been reported in these patients, but there is no tumor-agnostic approval.
Resistance: why do the drugs stop working?
In the large majority of patients who respond to KRAS G12C inhibitors, the disease eventually progresses again. In about one third of patients, the drug is ineffective from the start (primary resistance). Resistance mechanisms fall into several groups (how cancer cells develop resistance to treatment):
- New changes in KRAS itself: Secondary mutations that disrupt the pocket where the drug binds (for example, Y96D), amplification of KRAS G12C, or the emergence of other KRAS mutations such as G12D or G12V.
- Activation of bypass pathways: MET or EGFR amplification, NRAS, BRAF or MAP2K1 mutations, and fusions such as RET or ALK.
- Change in tissue type: Transformation of adenocarcinoma into squamous cell carcinoma.
- Unfavorable co-mutations: KEAP1 and STK11 mutations and overactivity of the NRF2 pathway reduce the response both to KRAS G12C inhibitors and to immunotherapy.
Three approaches are being pursued to overcome resistance: more potent second-generation drugs (divarasib, olomorasib), drugs that target the on state of KRAS (elironrasib), and combinations (with SHP2, SOS1, FAK, EGFR or MEK inhibitors). In an early-phase study of 24 patients previously treated with a KRAS G12C inhibitor, elironrasib achieved a response rate of 42% and a median progression-free survival of 6.2 months; it received Breakthrough Therapy designation from the FDA for patients who have not received a first-generation drug.
Treatment sequence as of 2026
Figure 4 · Treatment pathway in advanced KRAS G12C-mutated lung cancer (October 2026)
General roadmap; choices depend on the patient and on access
Sotorasib (Lumykras) is licensed in Turkey; the Turkish Oncology Group's real-world study shows that the drug is reaching patients in Turkey. However, a large share of newly licensed cancer drugs are not covered by the SGK (Turkish Social Security Institution) and in practice can be obtained only by paying out of pocket or through legal action; for the reimbursement status of sotorasib, you should consult your physician and the SGK's current list. Adagrasib (Krazati) is not licensed in Turkey, and there does not appear to be a routine import channel. Divarasib, olomorasib and elironrasib are not yet approved in any country; fulzerasib, garsorasib and glecirasib, which are approved in China, are also not available in Turkey. The route to these drugs is through clinical trials. For details, see our article FDA-approved new cancer drugs: Turkey access map.
Advice for patients and their families
- Ask for molecular testing: Every patient diagnosed with lung adenocarcinoma or metastatic colorectal cancer should have comprehensive molecular testing, including KRAS. A KRAS G12C result is assessed together with other targets such as EGFR, ALK or HER2 (biopsy).
- Ask about co-mutations: STK11 and KEAP1 results can affect the choice of treatment and the expected response.
- Take care right after immunotherapy: If a KRAS G12C inhibitor is started shortly after immunotherapy, liver tests need to be monitored closely.
- Report diarrhea early: Diarrhea, nausea and liver side effects can usually be managed with dose adjustments.
- Ask about clinical trials: First-line trials and trials of new drugs such as divarasib are currently the only way to access these drugs (what is a phase 1 clinical trial).
- Quit smoking and stay active: Even after diagnosis, quitting smoking and regular exercise support treatment adherence and quality of life (exercise in lung cancer).
For the symptoms and stages of lung cancer, see our general guide; for recent approvals, our article on FDA approvals that changed lung cancer treatment in 2025; and for other targetable alterations, our articles on ALK-positive and EGFR PACC-mutated lung cancer. For pancreatic cancer, our pancreatic cancer guide, and for monitoring with tumor DNA in the blood, our article on the ctDNA test may be helpful.
Frequently asked questions
- What is the KRAS G12C mutation?
- A change in the KRAS gene in which the glycine at position 12 of the protein is replaced by cysteine, so the protein keeps the growth signal constantly switched on. It is found in about 13% of lung adenocarcinomas, 3–4% of colorectal cancers and 1–2% of pancreatic cancers. Tablet drugs that target this mutation are available.
- How effective are sotorasib and adagrasib?
- In previously treated lung cancer, response rates are 30–40% and median progression-free survival is 5.5–6.8 months. In phase 3 trials, they modestly prolonged progression-free survival compared with docetaxel (5.6 vs 4.5 months and 5.5 vs 3.8 months), but no overall survival benefit was shown.
- What did the Krascendo 1 trial show?
- In Krascendo 1, presented at ESMO 2026 and published in NEJM, divarasib increased median progression-free survival from 5.7 to 9.8 months (HR 0.58) and median overall survival from 12.0 to 17.7 months (HR 0.56) compared with sotorasib or adagrasib. Serious adverse events were less frequent. Divarasib is not yet approved.
- Are KRAS G12C inhibitors available in Turkey?
- Sotorasib is licensed in Turkey; its reimbursement status should be discussed with your physician. Adagrasib is not licensed. Access to new drugs such as divarasib and olomorasib is possible only through clinical trials.
Glossary
- KRAS
- A protein that regulates cell growth and works like an on/off switch, and the gene that encodes it.
- G12C
- Replacement of the glycine at position 12 of the KRAS protein by cysteine; the KRAS subtype to which drugs can bind.
- Covalent inhibitor
- A drug that attaches to its target protein with a permanent bond.
- OFF / ON inhibitor
- Drugs that bind to KRAS in its off (GDP-bound) or on (GTP-bound) state.
- Pan-RAS inhibitor
- A drug that targets different RAS mutations without being limited to a specific one; for example, daraxonrasib.
- EGFR antibody
- Drugs such as panitumumab and cetuximab used in colorectal cancer; they are given together with KRAS G12C inhibitors to enhance their effect.
- Accelerated approval
- A conditional FDA approval granted on the basis of early data and dependent on the results of a confirmatory trial.
- Co-mutation
- Other genetic alterations present in the same tumor together with the main mutation; for example, STK11 and KEAP1.
DROZDOGAN Academy Commentary
The KRAS G12C story is a fine example of how basic science can change clinical practice; but it is also a reminder that a first success does not always translate into a large clinical gain.
⚡ Why it matters
Krascendo 1 is the first randomized phase 3 trial to show that a targeted drug prolongs overall survival in KRAS G12C-mutated lung cancer. A head-to-head comparison of two drugs directed at the same target is also uncommon in oncology.
✅ Strengths
Global, randomized design; independent review committee assessment; comparison with active, approved drugs; superiority in both efficacy and side effects; and publication in NEJM.
⚠️ Limitations
The first-generation drugs did not prolong overall survival compared with docetaxel; in colorectal cancer, KRYSTAL-10 was negative. Krascendo 1 was open-label, few patients in the control arm received adagrasib, and untreated brain metastases were excluded. First-line phase 3 results are not yet available.
🩺 In practice
Testing for KRAS and co-mutations at diagnosis is essential. In Turkey today, sotorasib is an option in the second line; if divarasib is approved, the standard may change. In colorectal cancer, a KRAS G12C inhibitor should be considered together with an EGFR antibody in chemotherapy-refractory patients.
❓ Open questions
Should KRAS G12C inhibitors move into the first line? Is combination with immunotherapy safe? What is the best treatment for patients with KEAP1 and STK11 mutations? Will drugs that target the on state and pan-RAS drugs solve the problem of resistance?
Bottom line: KRAS G12C is no longer "undruggable," but the effect of the first-generation drugs was limited. At ESMO 2026, Krascendo 1 showed that the second-generation drug divarasib can deliver a meaningful gain in survival. The next big question is whether these drugs will find a place in the first line.
- This article was prepared in October 2026.
- The data were compiled from published phase 1–3 trials, news reports and company statements on ESMO 2026 presentations, and FDA decisions. The full text of the Krascendo 1 article was not accessed; overall survival data from KRYSTAL-12 are not included in this article.
- Some charts show results from different trials together; in these charts, the comparison is indirect. In each trial, the experimental arm is shown in color and the control arm in gray.
- Information on licensing and reimbursement in Turkey reflects the date of writing and may change.
- This article is for general information only and is not personal medical advice. The diagrams are derived from the text and contain no new data. The Academy commentary is our own.
References
- Ostrem JM, Peters U, Sos ML et al. K-Ras(G12C) inhibitors allosterically control GTP affinity and effector interactions. Nature 2013;503:548-51. doi:10.1038/nature12796
- Skoulidis F et al. Sotorasib for lung cancers with KRAS p.G12C mutation (CodeBreaK 100). N Engl J Med 2021;384:2371-81. doi:10.1056/NEJMoa2103695
- Jänne PA et al. Adagrasib in non–small-cell lung cancer harboring a KRAS G12C mutation (KRYSTAL-1). N Engl J Med 2022;387:120-31. doi:10.1056/NEJMoa2204619
- de Langen AJ et al. Sotorasib versus docetaxel for previously treated non-small-cell lung cancer with KRAS G12C mutation (CodeBreaK 200). Lancet 2023;401:733-46. doi:10.1016/S0140-6736(23)00221-0
- Barlesi F, Mok TSK et al. Adagrasib versus docetaxel in KRAS G12C-mutated non-small-cell lung cancer (KRYSTAL-12). Lancet 2025. sciencedirect.com
- FDA issues complete response letter for sotorasib. CancerNetwork, January 2024. cancernetwork.com
- Sacher A et al. Single-agent divarasib (GDC-6036) in solid tumors with a KRAS G12C mutation. N Engl J Med 2023;389:710-21. doi:10.1056/NEJMoa2303810
- Skoulidis F et al. Divarasib versus sotorasib or adagrasib in KRAS G12C–mutated NSCLC (Krascendo 1). ESMO Congress 2026, LBA5; N Engl J Med 2026. doi:10.1056/NEJMoa2605703
- Details of the Krascendo 1 results. OncoDaily, October 25, 2026. oncodaily.com
- Lilly. New data on olomorasib at ESMO 2026. investor.lilly.com
- Updated KRYSTAL-7 data: adagrasib plus pembrolizumab, first line. AJMC, 2025. ajmc.com
- CodeBreaK 101: first-line sotorasib plus carboplatin-pemetrexed. ILCN, 2024. ilcn.org
- Fakih MG et al. Sotorasib plus panitumumab in refractory colorectal cancer with mutated KRAS G12C (CodeBreaK 300). N Engl J Med 2023;389:2125-39. doi:10.1056/NEJMoa2308795
- FDA approves sotorasib with panitumumab for KRAS G12C-mutated colorectal cancer. FDA, January 2025. fda.gov
- FDA withdraws Krazati plus Erbitux approval in KRAS G12C-mutated colorectal cancer (KRYSTAL-10). CURE, September 2026. curetoday.com
- Strickler JH et al. Sotorasib in KRAS p.G12C–mutated advanced pancreatic cancer. N Engl J Med 2023;388:33-43. doi:10.1056/NEJMoa2208470
- Awad MM et al. Acquired resistance to KRAS G12C inhibition in cancer. N Engl J Med 2021;384:2382-93. doi:10.1056/NEJMoa2105281
- Revolution Medicines. Updated elironrasib data after prior KRAS G12C(OFF) inhibitor. October 2025. ir.revmed.com
- Glecirasib NMPA approval. Jacobio, May 2025. jacobiopharma.com
- Fulzerasib NMPA approval. synapse.patsnap.com
- Akdoğan O et al. Multicenter real-world experience from the Turkish Oncology Group: sotorasib in KRAS G12C-mutated NSCLC. Eurasian J Med Invest 2024;8(4):274-9. turkmedline.net
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