Red Sun Medizone Launches CE-Marked EGFR Mutation PCR Kit for Seven-Target Genotyping of Exons 18-21 in NSCLC Tissue to Guide TKI Therapy

September 29, 2026

EGFR Mutation PCR Panel: Seven-Reaction ARMS Real-Time PCR Genotyping of Exons 18–21 in Tumour Tissue to Guide First-Line TKI Selection and Resistance Testing in Non-Small Cell Lung 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 EGFR gene mutations in exons 18, 19, 20 and 21 in tumour tissue. The kit is intended to select patients with non-small cell lung cancer (NSCLC) for whom EGFR tyrosine kinase inhibitor (TKI) therapy is indicated. Seven mutation-specific reactions — G719X, S768I, T790M, L858R, L861Q, DEL19 and INS20 — are read from a single 8-tube strip per specimen, in one laboratory day, on a standard real-time PCR platform with no sequencing queue and no new capital equipment.

Molecular pathology workbench with paraffin-embedded tumour tissue blocks, stained glass slides and a real-time PCR instrument used for EGFR mutation testing in non-small cell lung cancer tissue

Key facts at a glance

Analytes: seven mutation classes across EGFR exons 18–21 — G719X (exon 18); DEL19 (exon 19); S768I, T790M and INS20 (exon 20); L858R and L861Q (exon 21)
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 assay-specific cut-off (8 or 10)
Limit of detection: 1% mutant allele in a wild-type background
Repeatability: Ct coefficient of variation ≤ 5% across ten parallel replicates at 1% and at 50% mutation concentration
Agreement: 100% positive agreement across the covered mutation references; 100% negative agreement against wild-type human genomic DNA
Sample input: ≤ 50 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: the genotype, not the histology, picks the drug

Lung cancer is the most frequently diagnosed cancer and the leading cause of cancer death worldwide [1]. In advanced NSCLC the treatment decision at diagnosis turns on a molecular question rather than a histological one: is the tumour EGFR-mutant, and if so which mutation? In the IPASS trial, among 261 patients positive for an EGFR mutation, progression-free survival was significantly longer with gefitinib than with carboplatin plus paclitaxel (hazard ratio 0.48, 95% CI 0.36–0.64, P<0.001), while the mutation-negative subgroup did not show that benefit [4]; the EURTAC trial demonstrated the same principle for erlotinib in European patients with EGFR mutation-positive disease [5]. The mutation report therefore has to be in hand before the first cycle is chosen.

The pre-test probability varies enormously with geography and patient characteristics, which is precisely why testing is universal rather than selective. A systematic review and meta-analysis of 456 studies covering 115,815 patients with NSCLC reported an overall pooled EGFR mutation prevalence of 32.3% (95% CI 30.9–33.7), ranging from 38.4% (36.5–40.3) in China to 14.1% (12.7–15.5) in Europe. Prevalence was higher in women than men (43.7% versus 24.0%), in non-smokers than in past or current smokers (49.3% versus 21.5%), and in adenocarcinoma than in non-adenocarcinoma histology (38.0% versus 11.7%) [2].

The value of getting the genotype right has risen with each generation of therapy. In the FLAURA trial, first-line osimertinib achieved a median progression-free survival of 18.9 months versus 10.2 months for standard first-generation EGFR-TKIs (hazard ratio 0.46, 95% CI 0.37–0.57) [6], and the final overall survival analysis reported 38.6 months versus 31.8 months (hazard ratio 0.80, 95% CI 0.64–1.00) [7]. At progression on a first- or second-generation TKI, the AURA3 trial showed that in T790M-positive disease osimertinib achieved a progression-free survival of 10.1 months versus 4.4 months for platinum plus pemetrexed (hazard ratio 0.30, 95% CI 0.23–0.41) [8] — making T790M status a routine second-line question, not an academic one. More recently, the PAPILLON trial established that exon 20 insertion disease, historically insensitive to first- to third-generation TKIs, responds to an amivantamab-based regimen with a median progression-free survival of 11.4 months versus 6.7 months (hazard ratio 0.40, 95% CI 0.30–0.53) [10].

Where the chain breaks is specimen adequacy, not intent. Across the osimertinib clinical programme, 4,864 biopsies and 2,402 resections were assessed: 91% were adequate for EGFR testing, but 12% of biopsies were inadequate — mainly because of insufficient tumour content (42% of inadequate biopsies) and insufficient tissue volume (35%) — rising to 10–15% in first-line advanced or metastatic disease and 16% in unresectable stage III, versus only 3% in resectable early-stage disease [14]. Small biopsies and cytology specimens represent more than 80% of the diagnostic material available in routine practice [15], so an assay that works at low input and low tumour content is a workflow requirement rather than a refinement. Real-world testing quality remains a live issue: a 2026 report on biomarker testing for NSCLC in community practices operated by an academic cancer centre found continued gaps in testing completion [20].

What the assay detects: the mutations that change treatment

EGFR is a receptor tyrosine kinase. Activating mutations in its kinase domain hold the receptor in a permanently "on" state without ligand, driving proliferation through the PI3K–AKT and MAPK pathways. The mutation also alters the adenosine-triphosphate binding pocket of the intracellular domain, which is why the mutant receptor binds gefitinib more strongly than the wild type — mutation and drug response are physically linked [3].

Mutation	Exon	Approx. share of EGFR mutations	Clinical meaning
Exon 19 deletion (DEL19)	19	~45%	Classic sensitising mutation; strongest TKI response class
L858R	21	40–45%	Classic sensitising point mutation
G719X	18	~5%	Uncommon sensitising mutation
L861Q	21	Uncommon	Uncommon sensitising mutation
S768I	20	Uncommon	Uncommon sensitising mutation, frequently compound
Exon 20 insertion (INS20)	20	~1–2% of EGFR mutations	Insensitive to first- to third-generation TKIs; addressed by amivantamab-based regimens
T790M	20	Up to ~50% of acquired resistance	Resistance mutation after first- or second-generation TKI; treatable with a third-generation agent

Source: mutation shares and clinical interpretation as stated in the product instructions for use; T790M as the principal mechanism of acquired resistance was first characterised by Kobayashi et al. [9]; exon 20 insertion treatment context from the PAPILLON trial [10].

DNA double helix with highlighted mutation sites overlaid on a semi-transparent illustration of human lungs, illustrating EGFR exon 18 to 21 mutations as predictive biomarkers in non-small cell lung cancer

How the assay works

Allele-specific priming. An ARMS primer sits directly over the mutation site. When the primer and target sequence match perfectly, amplification proceeds efficiently; a single-base mismatch blocks it. Specificity is therefore enforced at the primer, before any signal is generated.

Hydrolysis-probe readout. A TaqMan probe on the same amplicon releases fluorescence only when the specific product is amplified, so signal reflects the intended target rather than any product. HotStart Taq DNA polymerase suppresses mis-priming before activation, adding a second specificity layer in a single 25 µL reaction.

Relative quantification by ΔCt. The mutation reaction is normalised against an external-standard reaction run on the same DNA extract: ΔCt = [mutation Ct] − [external-standard Ct]. Because the normalisation is against the specimen's own DNA, under- and over-loaded samples become visible in the result rather than silently distorting it. The external-standard Ct is expected between 14 and 28; outside that window the DNA is judged excessive (Ct ≤ 14) or deficient or inhibited (Ct ≥ 28) and the specimen is re-processed.

Controls are part of the run. An internal control monitors every individual tube; a positive control (plasmid clones of the covered mutations) and a negative control (purified wild-type human genomic DNA) are processed with every clinical batch. A specimen result is only reported once validity has been established: the internal control must rise, the negative control must show no clear FAM signal or a ΔCt above threshold, and the positive control must show a clear FAM signal with a ΔCt below threshold.

Reading the result: assay-specific cut-offs

No.	Reaction	Exon	Cut-off ΔCt	Positive call
1	G719X	18	8	S-shaped curve and ΔCt ≤ 8
2	S768I	20	10	S-shaped curve and ΔCt ≤ 10
3	T790M	20	8	S-shaped curve and ΔCt ≤ 8
4	L858R	21	10	S-shaped curve and ΔCt ≤ 10
5	L861Q	21	10	S-shaped curve and ΔCt ≤ 10
6	DEL19	19	10	S-shaped curve and ΔCt ≤ 10
7	INS20	20	10	S-shaped curve and ΔCt ≤ 10

Source: product instructions for use, version V2.2 (effective November 2024). Cut-offs are assay-specific and must not be transferred between products or reagent lots.

Workflow and logistics

One 8-tube strip is used per specimen — seven mutation reactions plus the external standard — with positive and negative controls on every plate. Up to ten patient specimens can be run on a 96-well plate alongside the controls. The thermal profile is 95 °C for 10 minutes for one cycle, then ten cycles of 95 °C for 15 seconds and 60 °C for 30 seconds, then 35 cycles of 95 °C for 15 seconds and 57 °C for 32 seconds, with FAM and HEX/VIC fluorescence collected at 57 °C.

Specimen handling follows a defined window: tissue is valid for 7 days at room temperature, 2 months at 2–8 °C and 6 months at ≤ –20 °C before extraction, and tolerates up to five freeze–thaw cycles. 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 operational notes matter in practice. First, a specimen may carry two mutations and amplify in more than one reaction tube; the instructions for use explicitly anticipate this and state that it does not affect the selection or the outcome of treatment. Second, a failed internal control triggers re-extraction or a new kit — except where a strong FAM signal has suppressed the HEX/VIC channel, in which case the result remains credible.

Analytical performance

Limit of detection. 1% mutant allele in a wild-type background. Mutation reference standards were assayed in a wild-type background, and the instructions for use state that detection of each covered mutation should be no lower than 1%.
Repeatability. Ct coefficient of variation ≤ 5%, established by assaying standardised references in ten parallel replicates at both 1% and 50% mutation concentration.
Positive agreement. Twenty mutation references assayed at 50% concentration; every covered mutation was detected.
Negative agreement. Wild-type human genomic references assayed; all results negative.
Internal control. HEX or VIC signal rises in every valid tube, monitoring amplification failure and PCR inhibition tube by tube.
External standard window. 14 < Ct(external standard) < 28; outside this window the specimen is re-processed.
Robustness. Five freeze–thaw cycles verified; nine-month shelf life at ≤ –20 °C in the dark.

Every figure in this section is taken from the product's own instructions for use, version V2.2, and is reproducible from the performance section of that document. No figure here is drawn from marketing material.

What the current documentation shows — and what it does not

It is worth stating this plainly, because a laboratory qualifying a supplier is better served by an honest evidence map than by an unqualified claim.

Evidence element	Status in the current documentation	What a laboratory should request
Analytical validation	Documented: limit of detection, repeatability, positive and negative agreement, controls	Available now in the instructions for use
Clinical concordance study	Not reproduced in the current instructions for use	Request the clinical evaluation dossier before tender submission
Method comparison reference	DNA sequencing is named as the comparison method in this product family	Confirm the exact comparator, sample count and blinding for this panel
Specimen types covered	Tumour tissue — fresh, frozen and paraffin-embedded	Confirm cytology-sample performance separately if you intend to use it
Variant list covered	Seven reactions across exons 18–21	Confirm coverage against local ordering patterns, especially exon 20 insertions

Source: product instructions for use, version V2.2. This table is presented as an evidence map, not as a performance claim.

The clinical claim rests on a simple chain: a 1% limit of detection and a ≤ 5% Ct variation mean the assay can report the mutations that change treatment at the allele fractions actually encountered in a small biopsy. Independent published evidence for the ARMS method on small specimens is summarised below.

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.

The treatment evidence that creates the intended use

IPASS established that EGFR mutation status determines whether a TKI outperforms chemotherapy: among 261 EGFR mutation-positive patients, progression-free survival was significantly longer with gefitinib than with carboplatin plus paclitaxel (hazard ratio 0.48, 95% CI 0.36–0.64, P<0.001), while mutation-negative patients did not show that benefit. (PMID 19692680) [4]
EURTAC confirmed the same principle for erlotinib as first-line therapy in European patients with advanced EGFR mutation-positive NSCLC. (PMID 22285168) [5]
FLAURA reported a median progression-free survival of 18.9 months with first-line osimertinib versus 10.2 months with standard EGFR-TKIs (hazard ratio 0.46, 95% CI 0.37–0.57), with a median duration of response of 17.2 versus 8.5 months. (PMID 29151359) [6]
The final FLAURA overall survival analysis reported a median overall survival of 38.6 months with osimertinib versus 31.8 months (hazard ratio 0.80, 95% CI 0.64–1.00). (PMID 31751012) [7]
AURA3 established the second-line T790M market: in T790M-positive advanced NSCLC after progression on a first- or second-generation TKI, osimertinib achieved a median progression-free survival of 10.1 months versus 4.4 months with platinum plus pemetrexed (hazard ratio 0.30, 95% CI 0.23–0.41), with an objective response rate of 71% versus 31%. (PMID 27959700) [8]
PAPILLON made a previously untreatable subset actionable: in NSCLC with EGFR exon 20 insertions, amivantamab plus chemotherapy achieved a median progression-free survival of 11.4 months versus 6.7 months with chemotherapy alone (hazard ratio 0.40, 95% CI 0.30–0.53), with 73% versus 47% objective response. (PMID 37870976) [10]
T790M was first characterised as the mechanism of acquired resistance to gefitinib by Kobayashi and colleagues, which is the basis for routine resistance testing at progression. (PMID 15728811) [9]
The biology linking EGFR mutations to TKI response — including the structural change in the ATP-binding pocket — was reviewed in Nature Reviews Cancer. (PMID 17318210) [3]

Marker prevalence and testing context

A systematic review and meta-analysis of 456 studies, including 30,466 patients with EGFR mutation among 115,815 patients with NSCLC, reported an overall pooled prevalence of 32.3% (95% CI 30.9–33.7), ranging from 38.4% in China to 14.1% in Europe, and higher in women, non-smokers and adenocarcinoma histology. (PMID 27738317) [2]
Across the osimertinib clinical programme, 91% of 7,266 tissue specimens were adequate for EGFR testing, but 12% of biopsies were inadequate — driven by insufficient tumour content in 42% and insufficient tissue volume in 35% of inadequate biopsies — rising to 10–15% in advanced or metastatic disease and 16% in unresectable stage III. (PMID 40311309) [14]
A two-year experience with 835 small diagnostic samples reported EGFR mutation testing failure in 5% of samples, associated with poor cellularity, low tumour cell percentage and poor DNA quality, and confirmed that small biopsies or cytology specimens represent more than 80% of available diagnostic material. (PMID 23628817) [15]
A 2026 review of biomarker testing for NSCLC in community practices operated by an academic cancer centre documents the continued real-world gap between guideline intent and testing completion. (PMID 41213102) [20]

Method performance on small specimens

A study of ARMS-based EGFR mutation analysis on cytological specimens and corresponding histological specimens reported 100% concordance between the two specimen types, and 100% concordance across 30 paired specimens from different sites (lung and pleural fluid) from the same patient. The authors concluded that cytology specimens are suitable when three conditions are met: DNA concentration above 2 ng/µL, more than 30 tumour cells, and a tumour percentage above 25%. This is the most directly relevant published evidence for an ARMS-based tissue assay. (PMID 25156817) [16]
A concordance study comparing fine-needle aspiration cell blocks with histological specimens for lung adenocarcinoma molecular testing reported comparable performance between the two preparation routes. (PMID 24987443) [17]

Guideline positions and the plasma question

The College of American Pathologists, the International Association for the Study of Lung Cancer and the Association for Molecular Pathology recommend EGFR testing for all patients with advanced lung adenocarcinoma, using validated assays with adequate sensitivity, and require that a negative result be reportable rather than assumed. (PMID 29398453) [11]
The ESMO Clinical Practice Guideline for oncogene-addicted metastatic NSCLC makes biomarker testing mandatory for drivers with approved therapies, and at progression on a first- or second-generation TKI recommends testing plasma cfDNA for T790M with re-biopsy where the plasma result is negative. (PMID 36872130) [12]
ESMO expert consensus statements caution that where ctDNA is used, a negative plasma result must be read with care because a proportion of patients do not shed detectable circulating tumour DNA, making a negative plasma result non-informative rather than negative — which is why tumour tissue remains the preferred specimen. (PMID 35176458) [13]
A 2025 review of strategies for clinical laboratories integrating ctDNA testing for EGFR analysis in advanced NSCLC sets out where plasma testing adds value and where tissue remains required. (PMID 40977812) [18]
A comparison of plasma next-generation sequencing and droplet digital PCR against tissue biopsy as the reference standard reported tissue-referenced sensitivity of 100% for NGS and 94% for ddPCR, with high concordance of allelic fractions — a reminder that plasma performance is measured against the tissue result. (PMID 31414729) [19]

Clinical use scenarios and who the test is for

First-line decision support

Where a non-squamous NSCLC is newly diagnosed and the choice between a TKI and platinum chemotherapy turns on the genotype. The panel returns the seven reactions most often ordered in routine thoracic practice in a single specimen run, inside one laboratory day.

Resistance testing at progression

Where a patient has progressed on a first- or second-generation TKI and T790M status decides whether a third-generation agent is available. A dedicated T790M reaction sits in the same strip as the sensitising-mutation reactions, so the second-line question can be answered from the same workflow.

Exon 20 insertion triage

Where an exon 20 insertion would change the regimen to an amivantamab-based one. An INS20 reaction flags the insertion class; confirmatory typing is appropriate where the exact insertion sequence affects the treatment decision.

Small-specimen pathways

Where the diagnostic material is a small biopsy or a cytology specimen — more than 80% of routine practice [15]. A 1% limit of detection and a ≤ 50 ng per-reaction input address the specimen reality that causes 12% of biopsies to be inadequate for testing [14].

Laboratories without a sequencing queue

Where rapid EGFR genotyping is needed ahead of therapy but next-generation sequencing capacity or turnaround is a constraint. Because the assay runs on FAM and HEX/VIC channels only, it maps onto the installed base of four-channel real-time PCR instruments.

Who this test is for. The kit is intended for laboratory directors and molecular pathology managers, molecular pathologists, thoracic oncologists, interventional pulmonology and cytopathology teams, 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 a broad genomic profiler. It does not interrogate ALK, ROS1, RET, MET exon 14, HER2, KRAS, BRAF or tumour mutational burden. Where guidelines require those markers, this panel runs alongside — not in place of — a broader assay.
It is not a plasma or ctDNA test. The intended use is tumour tissue. Where plasma testing is indicated, the guidelines themselves require a tissue step when plasma is negative, because a proportion of patients do not shed detectable circulating tumour DNA and a negative plasma result is non-informative rather than negative [12,13].
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 patient's condition.
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. A negative result from a specimen with low tumour content is not a reliable negative.
It reports mutation classes, not exact sequences. The INS20 reaction flags the exon 20 insertion class; where the precise insertion affects therapy, confirmatory typing is required.
The current instructions for use do not reproduce a clinical concordance study. Analytical validation is documented; a clinical concordance dataset for this specific panel should be requested from the supplier and reviewed before tender submission.
Cut-offs are assay- and lot-specific. The ΔCt thresholds of 8 and 10 apply to this product as stated in its instructions for use and must not be transferred to other assays or reagent lots.

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 evaluation dossier — is available to qualified laboratories on request.

Frequently asked questions

What does the test detect? The most prevalent EGFR mutations in exons 18, 19, 20 and 21 — G719X, DEL19, S768I, T790M, INS20, L858R and L861Q — in DNA extracted from tumour tissue, reported as mutation-positive or mutation-negative per reaction.

What sample is required? Tumour tissue, with fresh material preferred, then frozen tissue, then formalin-fixed paraffin-embedded blocks. The specimen must have been confirmed to contain tumour cells by the pathologist.

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. A positive call requires an S-shaped amplification curve and a ΔCt at or below the assay-specific cut-off, which is 8 for G719X and T790M and 10 for the remaining five reactions.

Can it be used on cytology specimens? The instructions for use specify tumour tissue. Published evidence for ARMS-based EGFR analysis reports 100% concordance between cytological and corresponding histological specimens when DNA concentration exceeds 2 ng/µL, tumour cell content exceeds 30 cells and tumour percentage exceeds 25% [16]. Laboratories intending to validate cytology specimens should do so locally.

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] Zhang YL, Yuan JQ, Wang KF, et al. The prevalence of EGFR mutation in patients with non-small cell lung cancer: a systematic review and meta-analysis. Oncotarget. 2016;7(48):78985-78993. doi:10.18632/oncotarget.12587. PMID 27738317.
[3] Sharma SV, Bell DW, Settleman J, Haber DA. Epidermal growth factor receptor mutations in lung cancer. Nat Rev Cancer. 2007;7(3):169-181. doi:10.1038/nrc2088. PMID 17318210.
[4] Mok TS, Wu YL, Thongprasert S, et al. Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma. N Engl J Med. 2009;361(10):947-957. doi:10.1056/NEJMoa0810699. PMID 19692680.
[5] Rosell R, Carcereny E, Gervais R, et al. Erlotinib versus standard chemotherapy as first-line treatment for European patients with advanced EGFR mutation-positive non-small-cell lung cancer (EURTAC): a multicentre, open-label, randomised phase 3 trial. Lancet Oncol. 2012;13(3):239-246. doi:10.1016/S1470-2045(11)70393-X. PMID 22285168.
[6] Soria JC, Ohe Y, Vansteenkiste J, et al. Osimertinib in Untreated EGFR-Mutated Advanced Non-Small-Cell Lung Cancer. N Engl J Med. 2018;378(2):113-125. doi:10.1056/NEJMoa1713137. PMID 29151359.
[7] Ramalingam SS, Vansteenkiste J, Planchard D, et al. Overall Survival with Osimertinib in Untreated, EGFR-Mutated Advanced NSCLC. N Engl J Med. 2020;382(1):41-50. doi:10.1056/NEJMoa1913662. PMID 31751012.
[8] Mok TS, Wu YL, Ahn MJ, et al. Osimertinib or Platinum-Pemetrexed in EGFR T790M-Positive Lung Cancer. N Engl J Med. 2017;376(7):629-640. doi:10.1056/NEJMoa1612674. PMID 27959700.
[9] Kobayashi S, Boggon TJ, Dayaram T, et al. EGFR mutation and resistance of non-small-cell lung cancer to gefitinib. N Engl J Med. 2005;352(8):786-792. doi:10.1056/NEJMoa044238. PMID 15728811.
[10] Zhou C, Tang KJ, Cho BC, et al. Amivantamab plus Chemotherapy in NSCLC with EGFR Exon 20 Insertions. N Engl J Med. 2023;389(22):2039-2051. doi:10.1056/NEJMoa2306441. PMID 37870976.
[11] Lindeman NI, Cagle PT, Aisner DL, et al. Updated Molecular Testing Guideline for the Selection of Lung Cancer Patients for Treatment With Targeted Tyrosine Kinase Inhibitors: Guideline From the College of American Pathologists, the International Association for the Study of Lung Cancer, and the Association for Molecular Pathology. J Mol Diagn. 2018;20(2):129-159. doi:10.1016/j.jmoldx.2017.11.004. PMID 29398453.
[12] Hendriks LE, Kerr KM, Menis J, et al. Oncogene-addicted metastatic non-small-cell lung cancer: ESMO Clinical Practice Guideline for diagnosis, treatment and follow-up. Ann Oncol. 2023;34(4):339-357. doi:10.1016/j.annonc.2022.12.009. PMID 36872130.
[13] Passaro A, Leighl N, Blackhall F, et al. ESMO expert consensus statements on the management of EGFR mutant non-small-cell lung cancer. Ann Oncol. 2022;33(5):466-487. doi:10.1016/j.annonc.2022.02.003. PMID 35176458.
[14] Murat-Onana ML, Ramalingam SS, Jänne PA, et al. EGFR mutation testing across the osimertinib clinical program. Lung Cancer. 2025;204:108549. doi:10.1016/j.lungcan.2025.108549. PMID 40311309.
[15] Hlinkova K, Babal P, Berzinec P, et al. Evaluation of 2-year experience with EGFR mutation analysis of small diagnostic samples. Diagn Mol Pathol. 2013;22(2):70-75. doi:10.1097/PDM.0b013e31827e6984. PMID 23628817.
[16] Liu J, Zhao R, Zhang J, et al. ARMS for EGFR mutation analysis of cytologic and corresponding lung adenocarcinoma histologic specimens. J Cancer Res Clin Oncol. 2015;141(2):221-227. doi:10.1007/s00432-014-1807-z. PMID 25156817.
[17] Heymann JJ, Bulman WA, Maxfield RA, et al. Molecular testing guidelines for lung adenocarcinoma: Utility of cell blocks and concordance between fine-needle aspiration cytology and histology samples. Cytojournal. 2014;11:12. doi:10.4103/1742-6413.132989. PMID 24987443.
[18] Fernández-Galán E, Puig-Butillé JA. Integrating ctDNA testing for EGFR analysis in advanced non-small cell lung cancer: strategies for clinical laboratories. Adv Lab Med. 2025;6(3):233-244. doi:10.1515/almed-2025-0012. PMID 40977812.
[19] Ding PN, Becker T, Bray V, et al. Plasma next generation sequencing and droplet digital PCR-based detection of epidermal growth factor receptor (EGFR) mutations in patients treated with osimertinib. Thorac Cancer. 2019;10(10):1879-1884. doi:10.1111/1759-7714.13154. PMID 31414729.
[20] Farhat K, Paul MA, Roby L, et al. Biomarker Testing for Non-Small Cell Lung Cancer in Community Practices Operated by an Academic Cancer Center. JCO Oncol Pract. 2026;22(9):1539-1545. doi:10.1200/OP-25-00280. PMID 41213102.

Note on sources: references [1]–[20] are independent, publicly retrievable peer-reviewed publications or guideline documents. All analytical performance figures and the mutation cut-off table 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 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 EGFR panel joins the company's existing thoracic-oncology molecular line, which includes a CE-marked SHOX2 and RASSF1A DNA methylation PCR kit for lung-cancer testing and a CE-marked methylated SEPT9 blood test for colorectal cancer screening. Together these assays address three distinct 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.