Medical Oncologist
Targeted therapy
KRAS G12C Mutation: — The Target That Was Undruggable for 40 Years
For nearly 40 years, the KRAS G12C mutation had no targeted treatment. Oral KRAS G12C inhibitors are now approved — and molecular testing is how you find out whether this option applies to you.
Medically reviewed by Dr. Bharati Devi Gorantla, Medical Oncologist, MBBS · MD · DM (Adyar, Chennai) · ECMO · MRCP SCE (UK) · Last reviewed August 2026
- A specific subtype — KRAS G12C is not the same as any KRAS mutation. The subtype must be confirmed before eligibility can be decided.
- Now targetable — Oral KRAS G12C inhibitors are approved by regulators including the US FDA for certain cancer types.
- Testing is essential — A report that says KRAS mutant may not confirm G12C. Your team needs the specific subtype in writing.
- Guidance is evolving — NCCN, ASCO and ESMO continue to update recommendations as evidence in this area matures.
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KRAS G12C is a specific mutation in the KRAS gene, found most often in non-small cell lung cancer. Oral targeted drugs called KRAS G12C inhibitors — sotorasib and adagrasib — are now approved for this mutation. Your oncologist identifies it through molecular testing of your tumour tissue or a blood sample.
What is the KRAS G12C mutation?
KRAS is a gene that sends growth signals inside cells. A mutation at the G12C position locks those signals permanently on, driving cells to divide without stopping.
KRAS G12C is found most often in non-small cell lung cancer, particularly the adenocarcinoma subtype. It also appears in a proportion of colorectal and pancreatic cancers.
For nearly 40 years, no drug could bind to this protein. Its surface had no obvious attachment point, which led researchers to call it undruggable. KRAS G12C inhibitors work by finding a hidden pocket that only forms in the mutant version of the protein, leaving the normal version untouched.
What should you confirm when you have a KRAS G12C result?
- Confirm the exact subtype in writing — KRAS G12C, not just KRAS mutant or KRAS-positive
- Ask which cancer type and treatment line the result applies to in your situation
- Find out whether your prior treatment history affects eligibility for a KRAS G12C inhibitor
- Ask for the full molecular report, including any co-mutations found alongside KRAS G12C
- Ask whether a clinical trial is open for your cancer type if approved options do not yet apply to you
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Dr. C. Raghavendra Reddy
MBBS(Gold Medal), DNB(General Medicine), DM(Medical Oncology)(Gold Medal)
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Dr. Bharati Devi Gorantla
MBBS, MD(General Medicine), DM(Medical Oncology)(Adyar,Chennai), ECMO, MRCP SCE(UK)
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Dr. Owais Mohammed
MBBS, MD (General Medicine), DrNB (Medical Oncology), ECMO, MRCP SCE (Medical Oncology) (UK)
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MBBS, MS(General Surgery), M.Ch(Surgical Oncology), FMAS, FARIS(Ongoing)
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How do KRAS G12C inhibitors work, and what drugs are available?
KRAS G12C inhibitors are oral tablets taken daily. They bind to the mutant KRAS G12C protein and hold it in an inactive state, cutting off the growth signal the cancer depends on.
Sotorasib was the first agent in this class to receive US FDA approval, for non-small cell lung cancer after at least one prior treatment. Adagrasib was approved subsequently and has been studied in additional cancer types in early research settings.
Both drugs target the same mutation. They differ in their dosing schedules, side effect profiles, and the cancer types and treatment lines for which they currently hold regulatory approval.
Response rates in the approved settings are reported by NCCN and regulatory bodies as clinically meaningful for eligible patients. Your oncologist will advise which agent fits your situation and how to access it, including any cost-support programmes that may apply.
What does a KRAS G12C-positive result mean for your treatment?
A positive result identifies a targeted treatment option that did not exist until recently. It does not guarantee a particular outcome, but it opens a treatment pathway designed specifically for your mutation.
Not every KRAS G12C-positive patient is immediately eligible for a KRAS inhibitor. Your cancer type, stage, and prior treatment history all influence whether one is recommended now or considered at a later stage.
If a KRAS inhibitor is not yet recommended for your situation, ask your oncologist to explain why and whether that may change as treatment progresses. NCCN and ESMO guidance in this area continues to be updated as longer-term evidence becomes available.
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Common questions
Frequently asked questions
Is KRAS G12C the same as having a KRAS mutation?
No, and the difference matters for treatment. KRAS is a gene that can mutate in many ways. KRAS G12C is one specific change — a substitution at position 12 from glycine to cysteine — and the approved targeted drugs work only on that particular form. A report that says KRAS-mutant without specifying the subtype cannot confirm eligibility for a KRAS G12C inhibitor. Ask your oncologist to confirm the exact mutation from your molecular pathology report before assuming which treatments apply to you.
What is the difference between sotorasib and adagrasib?
Both are approved KRAS G12C inhibitors that bind to the mutant protein and block its signalling. They differ in dosing schedules, side effect profiles, and the specific cancer types and treatment lines for which they have regulatory approval. Your oncologist will choose based on your cancer type, treatment history, and what is accessible to you. Long-term comparative evidence between the two is still being gathered, so we do not yet know whether one is clearly better than the other for most patients.
Can I get KRAS G12C treatment in India?
Both sotorasib and adagrasib have regulatory approval in several countries, and access within India is developing. Your oncologist or hospital patient services team can advise on current availability, whether the drug can be accessed on a named-patient basis, and whether clinical trials are open for your cancer type. Cost and access change quickly, so discuss this directly with your treating team rather than relying on information sourced online, where details become outdated fast.
Does having KRAS G12C mean I cannot have chemotherapy?
No. KRAS G12C does not rule out chemotherapy. For many patients, chemotherapy remains part of the recommended treatment — sometimes before a KRAS inhibitor, sometimes in a different line. Your oncologist decides the sequence based on your cancer type, stage, and the current evidence. Having a targetable mutation is one piece of information in that decision, not a replacement for everything else your oncologist considers.
What side effects do KRAS G12C inhibitors cause?
Common side effects reported in clinical studies include diarrhoea, nausea, fatigue, and elevated liver enzyme levels. Some patients experience joint or muscle pain. Side effect profiles differ between sotorasib and adagrasib, and your oncologist will explain what to watch for with the specific agent you are prescribed. Because liver enzyme changes can be significant, blood tests are monitored regularly during treatment. Tell your team about any new symptom, including mild ones, rather than waiting for your next scheduled appointment.
How is KRAS G12C testing done?
Testing is done on tumour tissue, usually from the biopsy you have already had. The laboratory uses next-generation sequencing to identify mutations across multiple genes at once, including the specific KRAS subtype. A liquid biopsy — a blood test that detects circulating tumour DNA — is an alternative when tissue is insufficient or unavailable, though tissue testing remains the standard where possible. Results typically take one to two weeks. If your existing pathology report does not specify the KRAS subtype, ask your oncologist whether additional testing is needed.