Aptamers for cancer
Novel tools for cancer diagnosis and therapy
Aptamers are oligonucleotides that can fold into secondary or tertiary structures and bind to target molecules through three-dimensional complementarity. Aptamers bind to target molecules with the same specificity and affinity as antibodies and their many advantages, particularly their lack of immunogenicity, make them a promising tool for cancer diagnosis and therapy.
AMSBIO provides a broad range of aptamers with human target proteins linked to cancer.
Aptamers for cancer diagnosis and therapy
Aptamers have many advantages when compared to antibodies. Aptamers are easier to synthesise and have a comparatively short discovery time. Aptamers are also more stable, easier to chemically modify, more stable in harsh conditions and non-immunogenic. Taken together, these advantages make aptamers promising tools for the diagnosis and treatment of diseases, including cancer.
There are two major uses for aptamers in cancer therapy. Aptamers can be used as target antagonists by targeting and inhibiting cancer-specific molecules. Aptamers can also be used as delivery vehicles for therapeutics by specifically targeting cell membrane receptors on cancer cells. The aptamer-drug conjugates can bind to, and be internalised by cancer cells while avoiding damage to healthy cells.
Aptamers can also be used to identify cancer cells and can recognize cancer metabolites, differentiating cells, molecules affecting tumor behavior, or cancer biomarkers, and have a great potential for cancer diagnostics. Current mass spectrometry (MS) and antibody-based technologies for biomarker discovery have several drawbacks including cross-reactivity, poor reproducibility, complexity and high cost that can be overcome by aptamer-based technologies such as cell-SLEX (cell-based systematic evolution of ligands through exponential enrichment) which can be used to screen for aptamers that bind to cancer cell-surface protein biomarkers.
We offer aptamers targeting many human proteins linked to cancer.
|Target proteins (human)||Kd(nM)||Target proteins (human)||Kd(nM)|
|Akt1 / PKB alpha||0.50||Notch-1||3.36|
|Akt2 / PKB BETA||4.48||PDCD1 / PD-1 / CD279||1.00|
|Akt3 / PKBG||0.69||PDCD1 LG 1 / CD274 / B7-H1 / PDL1||17.98|
|Cathepsin B / APPS / CTSB / CPSB||1.16||PDCD1 LG 2 / PD-L2||4.87|
|CD118 / LIFR||0.67||PECAM1 / CD31||1.14|
|CD11a / Integrin αLβ2 / LFA1 / INaLb2||1.02||Plexin B3 / PLXNB3/ KIAA1206 / PLXN6||5.60|
|CD48 / BCM1 / SLAMF2 / BLAST-1||31.70||Plexin C1 / PLXNC1/ VESPR / CD232||0.08|
|CD81 (TAPA-1, TMSF)||6.38||PRKCI / GST-PKC-γ||80.74|
|CDH5 / 7B4||5.82||PRL R||3.70|
|CDH6 / KCAD||0.56||SCFR / c-kit / CD117 / KIT||0.03|
|CDHE / CDH1||0.22||SIGLEC5||1.29|
|CEACAM-5 / CEA / CD66e||12.34||SUMO1 / SMT3C / SMT3H3 / UBL1||0.33|
|CHL1 / CALL / L1-CAM2||0.72||TGF beta R III||79.26|
|DDR1 / CD167A||4.14||TIE1 / Tie||10.10|
|EGFR / ErbB1 / HER-1 / ErbB||0.62||TIE2 / TEK||4.97|
|Endoglin / CD105 / ENG||60.62||TLR2 / CD282||6.70|
|EphB6||0.44||TNFR SF10A / TRAIL R1||0.11|
|FGF R1 alpha (IIIb)||15.70||TNFR SF10B / TRAIL R2 / DR5||2.21|
|FGF R1 alpha (IIIc)||0.82||TrkC / NTRK3||2.40|
|FGF R1 beta (IIIb)||17.69||VLA-5 / CD49e / INa5b1||1.47|
|FGF R1 beta (IIIc)||1.20||VSIG4 / CRIg / Z39IG||3.95|
|FLT-3 / FLK-2 / Stk-1||0.50||YES / GST-YES1||6.90|
|HMGB1 / HMG1 / Amphoterin||0.05||CD63 / MLA1 / TSPAN30||8.81|
|ICAM3 / CD50||0.17||CD66b / CEACAM8||3.50|
|IGF1 R / CD221||0.66||ErbB3 / Her3||0.30|
|IGSF4B / NECL1 / TSLL1 / CADM3 / SynCA||1.30||ErbB4 / Her4||5.60|
|IL3 R alpha / CD123 / IL3R||71.36||PDPN / GP36||85.74|
|IL6 R / CD126||0.57||TIGIT / VSIG9 / VSTM3||23.23|
|Legumain||0.92||PODXL / PCLP-1 / Gp200||1.54|
|MERTK / MER||8.82||SPHK1 / SK1 / SPK1||0.55|
|MPL / CD110 / TpoR||1.81||ICAM-1 / CD54||2.49|
|Mre11 & Rad50||0.17||EphA10||0.06|
|NCAM-1 / CD56||2.12|