PNA Clamp Kits

PNAClamp Technology is the PNA-based PCR clamping that selectively amplifies only the mutated target DNA sequence as a minor portion in the mixture with the major wild type DNA sequences. It takes full advantages of the nature of PNA probes that has strong binding affinity and specificity to its target DNA and not being recognized by DNA polymerase as primer.

PNAClamp Mutation detection kits can use DNA samples from surgical tissue or formalin-fixed paraffin-embedded biopsies (FFPE).

PNAClamp Mutation detection kits offer many advantages over conventional methods.

  • Mutation detected in a short time (3 hr run-time, 30 min hands-on time)
  • Simple protocol
  • Small amount of DNA sample (1~25 ng) needed for detection
  • High sensitivity (detection limit <1%)
  • Consistent
  • Long shelf life (>1 year)
  • Compatible with various real time PCR machines (ABI-7500, ABI-7900HT, Biorad CFX-96/384, Roche Lightcycler, Qiagen RGQ, etc)
  • Analysis software for simple data interpretation
  • We also provide dedicated technical support to set up and to analyze data.

    EGFR Mutation Details

    The epidermal growth factor receptor (EGFR) is a family member of Receptor tyrosine kinases, expressed on the surface of epidermal cells. Overexpression or overactivation of EGFR is linked to a number of cancers, including lung cancer, anal cancers and glioblastoma multiform.

    The PNAClamp EGFR Mutation Detection Kit detects most prevalent mutations described to date in the EGFR gene, including T790M, the presence of which correlates with resistance to tyrosine kinase inhibitors. Detecting somatic mutations in EGFR gene may provide a useful strategy to predict the response to the tyrosine kinase inhibitors in efforts to increase the survival rate of lung cancer patients receiving targeted therapy.

    < Mutations detected by PNAClamp EGFR Kit>

    ExonAmino acid changeBase change
    18Gly719Ala 2156 G>C
    Gly719Ser 2155 G>A
    Gly719Cys 2155 G>T
    19 Glu746_Ala750del 2235_2249 del 15
    Glu746_Thr751delinslle 2235_2252 AAT (complex)
    Glu746_Ser752del 2236_2253 del 18
    Glu746_Thr751delinsAla 2237_2251 del 15
    E746_S752>A 2237_2254 del 18
    Glu746_Ser752delinsVal 2237_2255 >T (complex)
    Glu746_Ala750del 2236_2250 del 15
    Glu746_Ser752delinsAsp 2238_2255 del 18
    L747_A750>P 2238_2248 >GC (complex)
    Leu747_Thr751delinsGln 2238_2252 >GCA (complex)
    Leu747_Glu749del 2239_2247 del 9
    Leu747_Thr751del 2239_2253 del 15
    Leu747_Ser752del 2239_2256 del 18
    Leu747_Glu749del:Ala750Pro 2239_2248 TTAAGAGAAG>C
    Leu747_Pro753delinsGln 2239_2258 >CA (complex)
    Leu747_Thr751delinsSer 2240_2251 del 12
    Leu747_Pro753delinsSer 2240_2257 del 18
    Leu747_Thr751del 2240_2254 del 15
    Leu747_Thr751deinsPro 2239_2251 >C (complex)
    20 Thr790Met 2369 C>T
    Ser768lle 2303 G>T
    Ala767_Val769dupAlaSerVal 2307_2308 ins9
    His773dupHis 2319_2320 insCAC
    Asp770_A771insGly 2310_2311 insGGT
    21 leu858Arg 2573 T>G
    leu861Gln 2582 T>A

    KRAS Mutation Details

    KRAS mutation is found in several cancers including colorectal, lung, thyroid, and pancreatic cancers and cholangiocarcinoma. KRAS mutations are often located within codons 12 and 13 of exon 2, which may lead to abnormal growth signaling by the p21-ras protein. These alterations in cell growth and division may trigger cancer development as signaling is excessive.

    A KRAS mutation often serves as a useful prognostic marker of drug response. For example, a KRAS mutation is considered to be a strong prognostic marker of response to tyrosine kinase inhibitors such as gefitinib (Iressa) or erlotinib (Tarceva). Recently, KRAS mutations have been detected in many colorectal cancer patients and may be associated with responses to cetuximab (Erbitux) or panitumumab (Vectibix), which are used in colon cancer therapy.

    < Mutations detected by PNAClamp KRAS Kit>

    Codon Mutation Base change
    Codon12 Gly12Asp 35G>A
    Gly12Ala 35G>C
    Gly12Val 35G>T
    Gly12Ser 34G>A
    Gly12Arg 34G>C
    Gly12Cys 34G>T
    Codon13 Gly13Ser 34G>T
    Gly13Arg 37G>C
    Gly13Cys 37G>T
    Gly13Asp 38G>A
    Gly13Ala 38G>C
    Gly13Val 38G>T
    Codon59 Ala59Ser 175G>T
    Ala59Thr 175GA
    Ala59Glu 176C>A
    Ala59Gly 176C>G
    Ala59del 176_178 del CAG
    Codon61 Gly60Asp 179G>A
    Gly60Ala 179G>C
    Gly60Val 179G>T
    Gly60Gly 180T>A
    Gly60Gly 180T>C
    Gln61Glu 181C>G
    Gln61Lys 181C>A
    Gln61Leu 182A>T
    Gln61Arg 182A>G
    Gln61Pro 182A>C
    Gln61His 183A>T
    Gln61His 183A>C
    Codon 117 Lys117Glu 349A>G
    Lys117Arg 350A>G
    Lys117Asn 351A>C
    Lys117Asn 351A>T
    Codon 146 Ala146Pro 436G>C
    Ala146Thr 436G>A
    Ala146Gly 437C>G
    Ala146Val 437C>T
    Ala146Ala 438A>G
    Ala146Ala 438A>C
    Ala146Ala 438A>T

    NRAS Mutation Details

    NRAS mutation is found in several cancers such as melanoma (13~25%), colorectal cancer(1~6%), lung cancer (1%), thyroid cancer (7%) and hepatocellular carcinoma (10%). It is knowthat the drug response against colorectal cancer medicine such as Erbitux and Cetuximabdecreased and the prognosis of the metastatic colorectal cancer patient is bad if the patient hasNRAS mutation.

    NRAS Mutation Details
     ยท PNAC-1101 (43 mutations)
    No.ReagentCodonAmino Acid ChangeNucleotide changeCosmic No.
    1N_G12 PNA
    mix

    2

    p.G12S
    c.34G>A563
    p.G12Rc.34G>C561
    p.G12Cc.34G>T562
    p.G12Nc.34_35GG>AA12723
    p.G12Pc.34_35GG>CC559
    p.G12Yc.34_35GG>TA560
    p.G12Dc.35G>A564
    p.G12Ac.35G>C565
    p.G12Vc.35G>T566
    2N_G13 PNA
    mix
    p.G13Sc.37G>A571
    p.G13Rc.37G>C569
    p.G13Cc.37G>T570
    p.G13Nc.37_38GG>AA24668
    p.G13Yc.37_38GG>TA568
    p.G13Dc.38G>A573
    p.G13Ac.38G>C575
    p.G13Vc.38G>T574
    p.G13Vc.38_39GT>TC572
    p.G13Gc.39T>C576
    3N_A59 PNA
    mix
    3p.A59Tc.175G>A578
    p.A59Dc.176C>A253327
    p.A59Gc.176C>G1178067
    4N_Q61 PNA
    mix
    p.Q61Kc.181C>A580
    p.Q61Ec.181C>G581
    p.Q61Rc.181_182CA>AG579
    p.Q61Lc.181_182CA>TT12725
    p.Q61Pc.182A>C582
    p.Q61Rc.182A>G584
    p.Q61Lc.182A>T583
    p.Q61Rc.182_183AA>GG33693
    p.Q61Lc.182_183AA>TG30646
    p.Q61Hc.183A>C586
    p.Q61Qc.183A>G587
    p.Q61Hc.183A>T585
    5N_K117 PNA
    mix
    4p.K117Ec.349A>G-
    p.K117Rc.350A>G-
    p.K117N_Tc.351G>T-
    p.K117N_Cc.351G>C-
    6N_A146 PNA
    mix
    p.A146Tc.436G>A27174
    p.A146Pc.436G>C-
    p.A146Sc.436G>T-
    p.A146Vc.437C>T-
    p.A146Gc.437C>G-
    1. Epidermal growth factor receptor pathway mutation and expression profiles in cervical squamous cell carcinoma: therapeutic implications. Bumrungthai S et al (2015) J Transl Med. 13:244.
    2. Impact of the Specific Mutation in KRAS Codon 12 Mutated Tumors on Treatment Efficacy in Patients with Metastatic Colorectal Cancer Receiving Cetuximab-Based First-Line Therapy: A Pooled Analysis of Three Trials. Modest DP et al. (2012)Oncology 83(5): 241-247.
    3. Association of KRAS p.G13D mutation with outcome in patients with chemotherapy-refractory metastatic colorectal cancer treated withcetuximab. De Roock W et al. (2010) JAMA 304(16): 1812-1820.
    4. Association of KRAS G13D tumor mutations with outcome in patients with metastatic colorectal cancer treated with first-line chemotherapy with or without cetuximab. Tejpar S et al. (2012) J Clin Oncol. 30(29): 3570-3577.
    5. Peptide nucleic acid-locked nucleic acid polymerase chain reaction clamp-based detection test for gefitinib-refractory T790M epidermal growth factor receptor mutation. Moyazawa H et al. (2008) Cancer Sci. 99(3): 595-600.
    6. Dissect Method Using PNA-LNA Clamp Improves Detection of EGFR T790M Mutation. Minakshi G et al. (2013) PLoS ONE. 8(6): e67782.
    7. Detection of EGFR Mutations in Archived Cytologic Specimens of Non-Small Cell Lung Cancer Using High-Resolution Melting Analysis. Nomoto K et al. (2006) Am J Clin Pathol. 126:608-615.
    8. High resolution melting analysis for rapid and sensitive EGFR and KRAS mutation detection informalin fixed paraffin embedded biopsies. Do H et al (2008) BMC Cancer. 8(142):1-14.

    BRAF mutation detection kit

    B-raf mutation is found in several cancers including thyroid cancer, malignant melanoma, ovarian cancer, colorectal cancer.

    ln case of thyroid cancer, there are over 40 different types of B-raf mutation. Of these mutations, V600E mutation on exon 15 (change from T to A in 1799th base) is most important with over 90% of frequency. Especially, B-raf V600E mutation is detected at about 45% of frequency in papillary thyroid carcinoma and is considered a prognostic maker for thyroid cancer.

    ln addition, the B-raf mutation in colorectal cancer is reported as a prognostic marker for reduced drug response to cetuximad(Erbitux) or panitumuab (Vectibix). These results imply that the B-raf mutation detection is needed for diagnosis and prognosis for drug response in colorectal and thyroid cancers.

    PI3K3CA Mutation Details

    PI3K (Phosphoinositide 3-kinases or PI 3-Kinases) are family of lipid kinases capable of phosphorylating the 3' position hydroxyl group of the inositol ring of phosphatidylinositol. They are involved in coordinating a diverse range of cell functions including cell growth, proliferation, differentiation, motility, survival and intracellular trafficking.

    Activating mutations in PI3K catalytic domain of the p110alpha subunit (PIK3CA) have recently been discovered in certain types of cancer cells. PIK3CA mutations are found at 25~40 % frequency in various types of tumors including colorectal cancer, gastric cancer, lung cancer, brain cancer, endometrial cancer, ovarian cancer, breast cancer. About 80% of the point mutations presides in exon 9 (a presumed helical domain) and exon 20 (a presumed kinase domain), while other types of mutations are also seen in different locations.

    < Mutations detected by PNAClamp PIK3CA Kit>

    Tube No Reagent Amino Acid Change Base change Exon Translation region
    1 E542 Glu542Lys 1624 G>A Exon 9 Helical
    Glu542Gly 1624 A>G
    Glu542Val 1624 A>T
    2 E545 Glu545Lys 1633 G>A
    Glu545Gly 1634 A>G
    Glu545Asp 1635 G>T
    3 H1047 His1047Tyr 3139 C>T Exon 20 Kinase
    His1047Leu 3140 A>T
    His1047Arg 3140 A>G

    IDH1 mutation detection kit

    Mutations of IDH1 (isocitrate dehydrogenase 1, IDH1) can be found in glioblastoma and myeloproliferative neoplasm.

    Detection of IDH1 mutations can be a positive predictor of a prognosis and a molecular marker for glioblasttoma patients. On the other hand, it is reported that IDH1 mutations correlate with poor prognosis in myeloproliferative neoplasm.

    PNAClamp IDH1 Mutation Detection Kit detects a mutation in R132 position with high sensitivity.

    Currently we are working on BCR-ABL (T315I, 944C>T) and JAK2 (V617F, 1849 G>T mutation)PNAClamp TM kits. We can also collaborate on custom genotyping development usingPNAClamp TM technology.

    Please feel free to inquire about any other kits that are not listed Contact us

    For quotation or order, please send us an email to order@pnabio.com.

    We usually respond within 6 hours after the inquiry was received. Also feel free to call at 805) 504-2220.

    Catalog NoProduct NameDescriptionSizePrice
    PNAC-1002PNAClamp KRAS Kit (v2)G12, G13 30 testsInquire
    PNAC-1003 PNAClamp KRAS Kit (v3) G12, G13, Q61 25 tests Inquire
    PNAC-1004 PNAClamp KRAS Kit (plus) A59, K117, A146 25 tests Inquire
    PNAC-1006 PNAClamp KRAS Kit (v4) G12, G13, A59, Q61, K117, A146 25 tests Inquire
    PNAC-1101 PNAClamp NRAS Kit (v4) G12, G13, A59, Q61, K117, A146 25 tests Inquire
    PNAC-2001 PNAClamp BRAF Kit BRAF V600 mutation 50 tests Inquire
    PNAC-3002 PNAClamp EGFR Kit G619, E19 del, T790, S768, E20 in, L858, L861 25 tests Inquire
    PNAC-4002 PNAClamp PIK3CA Kit E542, E545, H1047 25 tests Inquire
    PNAC-5001 PNAClamp IDH1 Kit R132 mutation 25 tests Inquire

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