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Red Sun Medizone Launches CE-Marked KRAS Mutation PCR Kit for Codon 12 and 13 Genotyping to Guide Anti-EGFR Therapy Decisions in Colorectal Cancer

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September 29, 2026

KRAS Codon 12/13 Mutation PCR Panel: Seven-Reaction ARMS Real-Time PCR Genotyping of Tumour Tissue to Determine Anti-EGFR Monoclonal Antibody Eligibility in Colorectal Cancer

HONG KONG, China — September 29, 2026 — Red Sun Medizone today announced the availability of a CE-marked in vitro diagnostic (IVD) real-time PCR kit for the detection of the most prevalent KRAS mutations in codons 12 and 13 in tumour tissue. The kit is intended to identify colorectal cancer patients whose tumours carry a KRAS mutation, a negative predictive finding for anti-EGFR monoclonal antibody therapy. Seven mutation-specific reactions — Gly12Asp, Gly12Val, Gly12Ser, Gly12Cys, Gly12Ala, Gly12Arg and Gly13Asp — are read from a single 8-tube strip per specimen, in one laboratory day, on a standard real-time PCR platform. In a three-centre registration study of 1,000 colorectal cancer specimens compared against DNA sequencing, the kit achieved 100% sensitivity, 99.26% specificity and a kappa agreement of 0.99.
Molecular pathology laboratory bench with a 96-well real-time PCR plate, paraffin-embedded colorectal tumour tissue blocks and stained histology slides used for KRAS codon 12 and 13 mutation testing

Key facts at a glance

  • Analytes: seven KRAS mutations in codons 12 and 13 — Gly12Asp (G12D, COSMIC 521), Gly12Val (G12V, 520), Gly12Ser (G12S, 517), Gly12Cys (G12C, 516), Gly12Ala (G12A, 522), Gly12Arg (G12R, 518) and Gly13Asp (G13D, 532)
  • Specimen: tumour tissue — fresh preferred, then frozen, then formalin-fixed paraffin-embedded (FFPE)
  • Chemistry: ARMS allele-specific PCR with TaqMan hydrolysis probes and HotStart Taq DNA polymerase
  • Detection channels: FAM (mutation and external-standard signal); HEX or VIC (internal control)
  • Reporting rule: ΔCt = [mutation Ct] − [external-standard Ct]; positive when the amplification curve is S-shaped and ΔCt is at or below the mutation-specific cut-off (8.5 or 10.0)
  • Limit of detection: 1% mutant allele against a 30 ng/µL wild-type genomic background
  • Repeatability: Ct coefficient of variation ≤ 5% across ten parallel replicates at 50% mutation proportion
  • Clinical verification: 1,000 colorectal cancer specimens across three tertiary referral centres against DNA sequencing — sensitivity 100%, specificity 99.26%, total coincidence 99.60%, kappa 0.99
  • Sample input: ≤ 300 ng DNA per reaction; extracted DNA OD260/280 between 1.6 and 2.0
  • Turnaround time: specimen to interpreted report inside one laboratory day
  • Kit configuration: 24 tests per kit — seven mutation reactions plus one external-standard reaction
  • Regulatory status: CE-marked IVD under Directive 98/79/EC, with an IVDR (EU) 2017/746 transition application; IVDR Class C, professional use

The clinical problem: a KRAS result is a treatment decision, not a diagnosis

Colorectal cancer is the third most commonly diagnosed cancer worldwide and the second leading cause of cancer-related death, with an estimated 1,926,425 new cases and 904,019 deaths globally in 2022 [2]. In metastatic disease, RAS genotyping is not an optional refinement — it determines whether an anti-EGFR monoclonal antibody is worth giving at all.
The predictive evidence is unambiguous. In the pivotal cetuximab study, 42.3% of evaluable tumours carried at least one KRAS exon 2 mutation, and the effectiveness of cetuximab was significantly associated with KRAS mutation status. Among patients with wild-type KRAS tumours, cetuximab compared with supportive care alone significantly improved overall survival (9.5 versus 4.8 months; hazard ratio for death 0.55, 95% CI 0.41–0.74) and progression-free survival (3.7 versus 1.9 months; hazard ratio 0.40, 95% CI 0.30–0.54). Among patients with mutated KRAS tumours there was no significant difference in outcome between cetuximab and supportive care alone (hazard ratio for death 0.98) [6].
The CRYSTAL trial extended this to first-line combination therapy: the progression-free survival hazard ratio among patients with wild-type KRAS tumours was 0.68 (95% CI 0.50–0.94) in favour of cetuximab plus FOLFIRI, with a statistically significant interaction between treatment group and KRAS mutation status for tumour response (P=0.03) [7]. In practice, roughly 30–40% of colorectal cancers carry a KRAS mutation [3], and one large consecutive series of 8,355 colorectal carcinomas detected KRAS mutations in 4,137 samples (49.5%), with NRAS mutations in a further 389 (4.7%) [4]. For every one of those patients, an anti-EGFR antibody is an expense and a toxicity burden with no expected benefit — and the only way to know is to test.
The guideline position is settled, and it defines the boundary of this assay. The joint ASCP/CAP/AMP/ASCO guideline requires RAS testing for any patient being considered for anti-EGFR therapy, covering KRAS and NRAS codons 12 and 13 of exon 2 together with codons 59 and 61 of exon 3 and codons 117 and 146 of exon 4 — the expanded RAS standard [5]. ASCO's provisional clinical opinion established KRAS testing before anti-EGFR monoclonal antibody therapy [9], and subsequent ASCO guidance formalised extended RAS analysis [10]. The ESMO consensus guidelines place RAS exon 2, 3 and 4 testing together with BRAF V600E at the time of metastatic diagnosis [11], and the Japanese Society of Medical Oncology guideline addresses RAS (KRAS/NRAS) testing specifically [16]. Every one of these documents treats KRAS codon 12/13 testing as necessary but not sufficient — a point this assay's limitations section addresses directly.

What the assay detects: the codons where the answer lives

KRAS is a small GTPase sitting immediately downstream of EGFR. Glycine residues at positions 12 and 13 are the contact points through which GTPase-activating proteins switch the protein off. Substituting either glycine locks KRAS in the active, GTP-bound state, so the MAPK and PI3K–AKT pathways remain switched on regardless of what happens at the receptor. Blocking EGFR upstream of a constitutively active KRAS achieves nothing — which is precisely why the mutation is a negative predictor rather than a prognostic curiosity [14]. KRAS mutation has also been reported as a poor prognostic feature in colorectal cancer independent of therapy [15].
ReactionMutationCOSMIC IDBase changeClinical note
K1Gly12Asp (G12D)521GGT>GATThe most frequent single substitution in colorectal cancer
K2Gly12Val (G12V)520GGT>GTTSecond most frequent substitution
K3Gly12Ser (G12S)517GGT>AGTCodon 12 substitution
K4Gly12Cys (G12C)516GGT>TGTNow potentially actionable with G12C-selective inhibitors
K5Gly12Ala (G12A)522GGT>GCTCodon 12 substitution
K6Gly12Arg (G12R)518GGT>CGTCodon 12 substitution
K7Gly13Asp (G13D)532GGC>GACThe dominant codon 13 substitution
Source: mutation list, COSMIC identifiers and base changes as stated in the product instructions for use, version V2.2, Table 1.
One consequence of testing at codon-level resolution rather than reporting a flat "KRAS mutant" result is worth noting. G12C now carries a specific therapeutic implication while the other codons do not. In the CodeBreaK100 phase 2 trial, sotorasib monotherapy in heavily pretreated KRAS G12C colorectal cancer produced an objective response in 9.7% of 62 patients (95% CI 3.6–19.9), which the authors reported as not reaching the efficacy benchmark and as supporting evaluation in combination [12]. In the KRYSTAL-1 trial, adagrasib monotherapy produced a response in 19% of 43 evaluable patients (95% CI 8–33) with a median progression-free survival of 5.6 months, while adagrasib plus cetuximab produced a response in 46% (95% CI 28–66) with a median progression-free survival of 6.9 months [13]. A report that names Gly12Cys therefore carries a different consequence from a report that names a codon 12 substitution generically — even though the treatment decision itself remains a clinical one.
DNA double helix with highlighted mutation sites overlaid on a semi-transparent illustration of the human colon, illustrating KRAS codon 12 and 13 mutations as predictive biomarkers in colorectal cancer

How the assay works

Allele-specific priming. An ARMS primer sits directly over the codon 12 or 13 base. A perfect primer–target match permits efficient amplification; a single-base mismatch blocks it. Specificity is therefore enforced at the primer, before any signal is generated.
Hydrolysis-probe readout. A TaqMan probe releases fluorescence only when the specific amplicon is generated, so signal comes from the intended target and nothing else. HotStart Taq DNA polymerase suppresses mis-priming before activation, adding a second specificity layer in a single 25 µL reaction.
Relative quantification by ΔCt. Each mutation reaction is normalised against an external-standard reaction run on the same DNA extract: ΔCt = [mutation Ct] − [external-standard Ct]. Because the normalisation uses the specimen's own DNA, under- and over-loaded samples are detected rather than hidden — a material advantage on paraffin-derived DNA, where input varies widely between blocks.
Controls are part of the run. The external-control reaction must fall between Ct 14 and 28; below 14 the DNA is judged excessive and diluted, at or above 28 the extract is deficient or inhibited and DNA is re-extracted. An internal control monitors every tube. A positive control (plasmids carrying the KRAS mutations) and a negative control (wild-type human genomic DNA) are processed with every clinical batch. A specimen result is reported only after validity has been established.

Reading the result: mutation-specific cut-offs

No.ReactionMutationCut-off ΔCtPositive call
1K1Gly12Asp≤ 8.5S-shaped curve and ΔCt ≤ 8.5
2K2Gly12Val≤ 10.0S-shaped curve and ΔCt ≤ 10.0
3K3Gly12Ser≤ 8.5S-shaped curve and ΔCt ≤ 8.5
4K4Gly12Cys≤ 10.0S-shaped curve and ΔCt ≤ 10.0
5K5Gly12Ala≤ 8.5S-shaped curve and ΔCt ≤ 8.5
6K6Gly12Arg≤ 8.5S-shaped curve and ΔCt ≤ 8.5
7K7Gly13Asp≤ 10.0S-shaped curve and ΔCt ≤ 10.0
Source: product instructions for use, version V2.2, Table 5. Cut-offs differ between reactions and must not be read as a single global threshold.

Workflow and logistics

One 8-tube strip is used per specimen — K1 to K7 plus the external standard — with positive and negative controls on every plate. The 96-well layout maps rows A to H to K1–K7 and the external standard, allowing up to ten patient specimens per plate alongside controls. The thermal profile is 95 °C for 10 minutes for one cycle, then ten cycles of 95 °C for 15 seconds and 62 °C for 30 seconds, then 35 cycles of 95 °C for 15 seconds and 60 °C for 32 seconds, with FAM and HEX or VIC fluorescence collected at 60 °C.
Sample input is up to 300 ng of DNA per reaction, with the DNA dose increased when the external-standard signal appears late. Extracted DNA is stored at ≤ –20 °C for a maximum of six months. The kit is stored at ≤ –20 °C in the dark with a nine-month shelf life, verified for five freeze–thaw cycles. Only FAM and HEX/VIC channels are required, so the assay maps onto the installed base of four-channel real-time PCR instruments — including the Roche LightCycler 480 and Applied Biosystems 7500 — without new capital equipment.
Two specimen-quality caveats are stated openly in the product documentation. Because of tumour heterogeneity, different sections from the same tumour may yield inconsistent results; and severely fragmented DNA from paraffin blocks may affect the outcome. Specimen quality, not the chemistry, is the dominant risk in this assay — which is why the instructions for use require the pathologist to confirm that the section used contains tumour cells.

Analytical performance

  • Limit of detection. 1% mutant allele against a 30 ng/µL wild-type genome background, established for all seven covered mutations.
  • Repeatability. Ct coefficient of variation ≤ 5%, established by assaying mixed references of all seven mutations at 50% mutation proportion in ten parallel replicates.
  • Positive reference agreement. References for Gly12Asp, Gly12Val, Gly12Ser, Gly12Cys, Gly12Ala, Gly12Arg and Gly13Asp at 50% mutation concentration were all detected.
  • Specificity against wild type. Wild-type human genomic references with no corresponding target mutation were all reported negative.
  • Specificity against off-panel and non-human DNA. Eight mutation references outside the detection range, and non-human genomic DNA (Staphylococcus aureus), were all reported negative.
  • External control window. 14 < Ct(external control) < 28; outside this window the specimen is diluted or re-extracted.
  • Controls. Positive control must be positive and negative control must be negative in every run; an internal control monitors each individual tube.

Clinical performance: the 1,000-specimen registration study

The product's clinical verification used DNA sequencing as the reference method and tested 1,000 colorectal cancer patient samples collected across three tertiary referral centres. Every specimen was assayed in parallel by the kit and by DNA sequencing, and the results were compared statistically.
Study elementAs documented
Reference methodDNA sequencing, run in parallel on every specimen
Specimens1,000 colorectal cancer patient samples, multi-centre, three tertiary referral centres
Mutation-positive callsDNA sequencing detected 456 mutant cases; the kit detected 459
Mutation-negative callsDNA sequencing detected 544 negative cases; the kit detected 541
Sensitivity100% against DNA sequencing
Specificity99.26% against DNA sequencing
Overall agreementKappa 0.99; total coincidence rate 99.60%
Source: product instructions for use, version V2.2, section "Specific Performance Characteristics — Clinical verification". Study centre names, specimen-level records and the complete technical dossier are available to qualified laboratories on request and are deliberately omitted from this communication.
Two points about this dataset deserve emphasis rather than glossing. First, kappa 0.99 against Sanger-class sequencing places the method comparison beyond the range at which a laboratory would normally question it — provided the specimens used match those in local practice. Second, the counts matter as much as the ratios: the two methods differed by three calls in each direction out of 1,000 specimens. That is the honest detail, and it is the correct standard by which to judge any supplier's concordance claim — the methods are not identical, they are statistically indistinguishable at this sample size.

Peer-reviewed evidence retrievable on PubMed

Every study below is retrievable on PubMed under the identifier given, and full citations with DOIs appear in the reference list.

KRAS as a negative predictor of anti-EGFR benefit

  • The pivotal cetuximab study found that among patients with wild-type KRAS tumours, cetuximab significantly improved overall survival (median 9.5 versus 4.8 months; hazard ratio for death 0.55, 95% CI 0.41–0.74) and progression-free survival (median 3.7 versus 1.9 months; hazard ratio 0.40, 95% CI 0.30–0.54), while among patients with mutated KRAS tumours there was no significant difference in overall survival between cetuximab and supportive care (hazard ratio 0.98). KRAS exon 2 mutations were present in 42.3% of evaluable tumours. (PMID 18946061) [6]
  • The CRYSTAL trial of first-line cetuximab plus FOLFIRI reported a progression-free survival hazard ratio of 0.68 (95% CI 0.50–0.94) in favour of the cetuximab arm among patients with wild-type KRAS tumours, with a significant interaction between treatment group and KRAS mutation status for tumour response. (PMID 19339720) [7]
  • The PRIME trial analysed panitumumab plus FOLFOX4: among 512 patients without RAS mutations, progression-free survival was 10.1 versus 7.9 months (hazard ratio 0.72, 95% CI 0.58–0.90) and overall survival 26.0 versus 20.2 months (hazard ratio 0.78, 95% CI 0.62–0.99). (PMID 24024839) [8]
  • ASCO's provisional clinical opinion recommended KRAS mutation testing for all patients with metastatic colorectal carcinoma before anti-EGFR monoclonal antibody therapy — the document that moved KRAS testing from research into routine practice. (PMID 19188670) [9]

The extended-RAS boundary — and why it matters for a codon 12/13 assay

  • The same PRIME analysis identified 108 of 512 patients (17%) with non-mutated KRAS exon 2 who carried other RAS mutations. Those additional mutations were associated with inferior progression-free and overall survival on panitumumab-FOLFOX4, consistent with the findings in patients with KRAS exon 2 mutations. (PMID 24024839) [8]
  • The joint ASCP/CAP/AMP/ASCO guideline requires expanded RAS testing covering KRAS and NRAS codons 12 and 13 of exon 2, codons 59 and 61 of exon 3, and codons 117 and 146 of exon 4 in any patient considered for anti-EGFR therapy. (PMID 28165299) [5]
  • Subsequent ASCO guidance formalised extended RAS gene mutation testing in metastatic colorectal carcinoma for predicting anti-EGFR response. (PMID 26443838) [10]
  • The Japanese Society of Medical Oncology clinical guideline addresses RAS (KRAS/NRAS) mutation testing in colorectal cancer patients, covering both genes. (PMID 25800101) [16]
  • The ESMO consensus guidelines for metastatic colorectal cancer recommend RAS exon 2, 3 and 4 testing together with BRAF V600E at the time of metastatic diagnosis. (PMID 27380959) [11]

Mutation frequency, G12C actionability and prognosis

  • A 2023 analysis of 8,355 consecutive colorectal carcinomas detected KRAS mutations in 4,137 samples (49.5%) and NRAS mutations in 389 (4.7%), with 3,913 of the KRAS mutations represented by ten common substitutions across codons 12, 13, 61 and 146. (PMID 36902296) [4]
  • A 2025 review reports KRAS mutations in 30–40% of colorectal cancers and examines their biological significance, prognostic impact and therapeutic targeting. (PMID 39941797) [3]
  • CodeBreaK100 evaluated sotorasib in heavily pretreated KRAS G12C colorectal cancer: objective response in 9.7% of 62 patients (95% CI 3.6–19.9), with the authors reporting that the response rate did not reach the benchmark and supporting evaluation in combination. (PMID 34919824) [12]
  • KRYSTAL-1 evaluated adagrasib alone and with cetuximab in KRAS G12C colorectal cancer: response in 19% of 43 evaluable patients on monotherapy (median progression-free survival 5.6 months) versus 46% of 28 evaluable patients on combination therapy (median progression-free survival 6.9 months), with grade 3 or 4 treatment-related adverse events in 34% and 16% respectively. (PMID 36546659) [13]
  • K-ras and p16 aberrations were reported to confer poor prognosis in human colorectal cancer, supporting the prognostic as well as predictive relevance of the marker. (PMID 11208819) [15]
  • The biology of hyperactive RAS in cancer and developmental disorders, including the switch-off mechanism disrupted by codon 12 and 13 substitutions, was reviewed in Nature Reviews Cancer. (PMID 17384584) [14]

Clinical use scenarios and who the test is for

First-line anti-EGFR eligibility

Where a metastatic colorectal cancer is newly diagnosed and the choice between an anti-EGFR monoclonal antibody and an anti-VEGF backbone turns on RAS status. The panel returns the codon 12/13 genotype from one specimen run, inside a working day, before the first infusion.

Reflex testing from the paraffin archive

Where the archival block is the only material available. Validated on paraffin-embedded tissue with an input of up to 300 ng per reaction, the assay runs on archived blocks alongside routine immunohistochemistry — the most common real-world workflow for colorectal molecular testing.

G12C identification

Where a named substitution changes the option set. A dedicated Gly12Cys reaction reports the variant directly rather than reporting "KRAS mutant", which matters now that G12C-directed combination regimens have shown activity [12,13]. Where a guideline advises further typing of a G12C or G12D result, this assay's codon-level reaction supports that step.

Fast front door before a broader panel

Where turnaround matters more than breadth on day one. Codons 12 and 13 cover the overwhelming majority of KRAS mutations; the remaining extended-RAS space is then addressed by a panel covering KRAS exons 3 and 4 and NRAS, rather than left untested [5,8].

Laboratories without sequencing capacity

Where RAS genotyping is needed but next-generation sequencing capacity, cost or turnaround is a constraint. Because the assay uses FAM and HEX/VIC channels only, it runs on the four-channel real-time PCR instruments already installed in most molecular laboratories.
Who this test is for. The kit is intended for laboratory directors and molecular pathology managers, molecular pathologists, gastrointestinal and medical oncologists, histopathology laboratory managers, hospital procurement teams and in-vitro diagnostics distributors. It is a laboratory test for professional use, not a direct-to-consumer product.

What this test is not

Any laboratory evaluating this assay should weigh its deliberate limits, which are stated in the instructions for use and reflected in the guideline literature.
  • It is not an extended-RAS assay — and this is the single most important limitation. It covers KRAS codons 12 and 13 only. It does not cover KRAS exon 3 (codons 59 and 61) or exon 4 (codons 117 and 146), and it does not cover NRAS at all. The joint ASCP/CAP/AMP/ASCO guideline requires expanded RAS testing covering all of those regions before anti-EGFR therapy is considered [5], and the PRIME trial found that 17% of patients with non-mutated KRAS exon 2 carried other RAS mutations that also predicted lack of benefit [8]. A negative result from this assay does not by itself establish RAS wild-type status. It must be confirmed by, or run alongside, a panel covering KRAS exons 3 and 4 and NRAS.
  • It is not a KRAS G12C response predictor on its own. The Gly12Cys reaction identifies the G12C variant, but G12C-directed therapy in colorectal cancer is used in defined combination regimens and remains a clinical decision [12,13].
  • It is not a BRAF assay. BRAF V600E is an adverse prognostic marker in colorectal cancer and is recommended alongside RAS testing [11]; where it is required, it must be tested separately.
  • It is not a stand-alone diagnosis. Results are a clinical reference and must not be the sole basis for an individual treatment decision; they are read with the histology, the stage and the treatment plan.
  • It does not replace the pathologist's adequacy assessment. The assay consumes DNA from a specimen that must already have been confirmed to contain tumour cells.
  • Tumour heterogeneity and DNA quality limit any result. The instructions for use state that different sections of the same tumour may give inconsistent results, and that severely fragmented paraffin-derived DNA may affect the outcome. A negative result from a specimen with low tumour content is not a reliable negative.
  • Cut-offs are mutation-specific and must not be generalised. The ΔCt thresholds of 8.5 and 10.0 apply per reaction as stated in the instructions for use, and must not be transferred to other assays or reagent lots.
  • It is not a plasma or liquid-biopsy assay. The intended use is tumour tissue. Where liquid biopsy is used, it is a complementary tool for monitoring emergent resistance rather than a replacement for the diagnostic tissue genotype.

Regulatory status, formats and availability

The kit is a CE-marked in vitro diagnostic device under Directive 98/79/EC, with an IVDR (EU) 2017/746 transition application lodged with a designated notified body; it is classified Class C for professional use. It is supplied as 24 tests per kit, comprising seven mutation-specific reaction mixes plus one external-standard reaction mix, together with HotStart Taq DNA polymerase, positive and negative controls and purified water. Full technical documentation — including the instructions for use, analytical performance data and the clinical verification dossier — is available to qualified laboratories on request.

Frequently asked questions

What does the test detect? Seven KRAS mutations in codons 12 and 13 — Gly12Asp, Gly12Val, Gly12Ser, Gly12Cys, Gly12Ala, Gly12Arg and Gly13Asp — in DNA extracted from tumour tissue, reported as mutation-positive or mutation-negative for each of the seven reactions.
What sample is required? Tumour tissue, with fresh material preferred, then frozen tissue, then formalin-fixed paraffin-embedded blocks. The pathologist must confirm that the section used contains tumour cells.
How long does it take? Specimen to interpreted report inside one laboratory day. The amplification programme runs approximately two hours after extraction, and up to ten patient specimens can be run per 96-well plate alongside controls.
What equipment is needed? A real-time PCR instrument with FAM and HEX/VIC channels, such as the Roche LightCycler 480 or Applied Biosystems 7500. No sequencing capacity and no additional capital equipment are required.
How is a result called? By ΔCt — the difference between the mutation reaction Ct and the external-standard reaction Ct run on the same DNA extract. A positive call requires an S-shaped amplification curve and a ΔCt at or below the mutation-specific cut-off, which is 8.5 for Gly12Asp, Gly12Ser, Gly12Ala and Gly12Arg and 10.0 for Gly12Val, Gly12Cys and Gly13Asp.
Can a negative result alone rule out RAS mutation? No. The assay covers KRAS codons 12 and 13 only. Expanded RAS testing under current guidelines also covers KRAS exon 3, KRAS exon 4 and NRAS, and 17% of patients with non-mutated KRAS exon 2 were found to carry other RAS mutations in the PRIME trial [8]. A negative result on this assay must be confirmed by a panel covering the remaining regions.
How was the assay validated? In a three-centre registration study, 1,000 colorectal cancer specimens were assayed in parallel by the kit and by DNA sequencing: sensitivity 100%, specificity 99.26%, total coincidence 99.60%, kappa 0.99.
Is it CE-marked? Yes — CE-marked as an in vitro diagnostic under Directive 98/79/EC, with an IVDR transition application and IVDR Class C classification for professional use.

References

Citation format: Vancouver (ICMJE). PubMed identifiers are given for every reference retrievable through PubMed.
  • [1] Bray F, Laversanne M, Sung H, et al. Global cancer statistics 2022: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 2024;74(3):229-263. doi:10.3322/caac.21834. PMID 38572751.
  • [2] Wu S, Zhang Y, Lin Z, Wei M. Global burden of colorectal cancer in 2022 and projections to 2050: incidence and mortality estimates from GLOBOCAN. BMC Cancer. 2025;25(1):1770. doi:10.1186/s12885-025-15138-0. PMID 41239247.
  • [3] Takeda M, Yoshida S, Inoue T, et al. The Role of KRAS Mutations in Colorectal Cancer: Biological Insights, Clinical Implications, and Future Therapeutic Perspectives. Cancers (Basel). 2025;17(3):428. doi:10.3390/cancers17030428. PMID 39941797.
  • [4] Martianov AS, Mitiushkina NV, Ershova AN, et al. KRAS, NRAS, BRAF, HER2 and MSI Status in a Large Consecutive Series of Colorectal Carcinomas. Int J Mol Sci. 2023;24(5):4868. doi:10.3390/ijms24054868. PMID 36902296.
  • [5] Sepulveda AR, Hamilton SR, Allegra CJ, et al. Molecular Biomarkers for the Evaluation of Colorectal Cancer: Guideline From the American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology, and American Society of Clinical Oncology. J Clin Oncol. 2017;35(13):1453-1486. doi:10.1200/JCO.2016.71.9807. PMID 28165299.
  • [6] Karapetis CS, Khambata-Ford S, Jonker DJ, et al. K-ras mutations and benefit from cetuximab in advanced colorectal cancer. N Engl J Med. 2008;359(17):1757-1765. doi:10.1056/NEJMoa0804385. PMID 18946061.
  • [7] Van Cutsem E, Köhne CH, Hitre E, et al. Cetuximab and chemotherapy as initial treatment for metastatic colorectal cancer. N Engl J Med. 2009;360(14):1408-1417. doi:10.1056/NEJMoa0805019. PMID 19339720.
  • [8] Douillard JY, Oliner KS, Siena S, et al. Panitumumab-FOLFOX4 treatment and RAS mutations in colorectal cancer. N Engl J Med. 2013;369(11):1023-1034. doi:10.1056/NEJMoa1305275. PMID 24024839.
  • [9] Allegra CJ, Jessup JM, Somerfield MR, et al. American Society of Clinical Oncology provisional clinical opinion: testing for KRAS gene mutations in patients with metastatic colorectal carcinoma to predict response to anti-epidermal growth factor receptor monoclonal antibody therapy. J Clin Oncol. 2009;27(12):2091-2096. doi:10.1200/JCO.2009.21.9170. PMID 19188670.
  • [10] Allegra CJ, Rumble RB, Schilsky RL. Extended RAS Gene Mutation Testing in Metastatic Colorectal Carcinoma to Predict Response to Anti-Epidermal Growth Factor Receptor Monoclonal Antibody Therapy. J Oncol Pract. 2016;12(2):180-181. doi:10.1200/JOP.2015.007898. PMID 26443838.
  • [11] Van Cutsem E, Cervantes A, Adam R, et al. ESMO consensus guidelines for the management of patients with metastatic colorectal cancer. Ann Oncol. 2016;27(8):1386-1422. doi:10.1093/annonc/mdw235. PMID 27380959.
  • [12] Fakih MG, Kopetz S, Kuboki Y, et al. Sotorasib for previously treated colorectal cancers with KRAS G12C mutation (CodeBreaK100): a prespecified analysis of a single-arm, phase 2 trial. Lancet Oncol. 2022;23(1):115-124. doi:10.1016/S1470-2045(21)00605-7. PMID 34919824.
  • [13] Yaeger R, Weiss J, Pelster MS, et al. Adagrasib with or without Cetuximab in Colorectal Cancer with Mutated KRAS G12C. N Engl J Med. 2023;388(1):44-54. doi:10.1056/NEJMoa2212419. PMID 36546659.
  • [14] Schubbert S, Shannon K, Bollag G. Hyperactive Ras in developmental disorders and cancer. Nat Rev Cancer. 2007;7(4):295-308. doi:10.1038/nrc2109. PMID 17384584.
  • [15] Esteller M, González S, Risques RA, et al. K-ras and p16 aberrations confer poor prognosis in human colorectal cancer. J Clin Oncol. 2001;19(2):299-304. doi:10.1200/JCO.2001.19.2.299. PMID 11208819.
  • [16] Taniguchi H, Yamazaki K, Yoshino T, et al. Japanese Society of Medical Oncology Clinical Guidelines: RAS (KRAS/NRAS) mutation testing in colorectal cancer patients. Cancer Sci. 2015;106(3):324-327. doi:10.1111/cas.12595. PMID 25800101.
Note on sources: references [1]–[16] are independent, publicly retrievable peer-reviewed publications or guideline documents. All analytical performance figures, the mutation table, the cut-off table and the 1,000-specimen clinical verification data are taken from the product's own instructions for use, version V2.2 (effective November 2024), which is product technical documentation held on file and is not independently peer reviewed; this is stated where those figures appear. Manufacturer names, trademarks, catalogue codes, certificate numbers, study centre names and authorised-representative details are deliberately omitted from this communication.

About Red Sun Medizone

Red Sun Medizone (RED SUN MEDI ZONE LIMITED) is a Hong Kong-based supplier of medical devices and in vitro diagnostic products serving hospitals, laboratories and distributors internationally. Its portfolio spans molecular diagnostics for oncology, critical-care and surgical equipment, patient monitoring, and laboratory instrumentation. The KRAS panel joins the company's existing molecular diagnostics line, which includes a CE-marked EGFR mutation PCR kit built on the same ARMS real-time PCR chemistry and platform, a CE-marked methylated SEPT9 blood test for colorectal cancer screening, and a CE-marked SHOX2 and RASSF1A DNA methylation PCR kit for lung-cancer testing. Together these assays address complementary molecular questions on one common real-time PCR platform.

Media and technical enquiries

Red Sun Medizone — Sales and Technical Enquiries
Mr. Matt Hou, Sales Manager
Email: [email protected]
Web: www.redsunmedizone.com
Unit 18, 8/F, Peter Leung Industrial Building, 103 Wai Yip Street, Kwun Tong, Hong Kong, China
This press release describes an in vitro diagnostic device intended for professional laboratory use. It is not a statement of clinical efficacy for any individual patient, and every performance figure quoted is drawn from the sources cited. The product is manufactured in accordance with CE-marked in vitro diagnostic requirements; manufacturing, regulatory and technical documentation is available to qualified purchasers on request.

Related reading: the somatic mutation PCR family

This kit belongs to a family of CE-marked real-time PCR assays for somatic mutation genotyping in formalin-fixed paraffin-embedded tissue. The other articles in the family cover:
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