S2.2 aptamer sodium 

S2.2 aptamer sodium is a nucleic acid-based MUC1-binding aptamer with high affinity and low toxicity. Upon binding to its target, S2.2 aptamer sodium undergoes a conformational switch and restores fluorescence signal, serving as a targeted imaging agent for MUC1-positive cancer cells. S2.2 aptamer sodium enables targeted delivery to breast cancer cells with overexpressed MUC1. When formulated as the S2.2-PEG-MZF molecular probe, S2.2 aptamer sodium possesses the functions of T2 signal inhibition, magnetic field-induced hyperthermia and targeted magnetic resonance molecular imaging. In the S2.2-PEG-MZF/DOX nanoliposome, S2.2 aptamer sodium supports targeted thermochemotherapy, effectively inhibiting cancer cell proliferation and invasion as well as inducing apoptosis, and is widely used in studies related to breast cancer^[1][2][3].

MUC1^[1]

After conjugation with SiND-Cy5, S2.2 aptamer sodium (100 μM, 32.5 mg, 150 μg/mL^-1, 3.33-250 nM; 5 min, 1.5 h, 12 h, 90 min) enables highly specific and sensitive turn-on fluorescence detection of MUC1 in cell-free samples, with a linear range of 3.33-250 nM and a limit of detection of 1.52 nM, and exhibits reliable performance in spiked human serum^[1].
After conjugation with SiND-Cy5, S2.2 aptamer sodium (0.15-1.02 mg/mL; 24 h) exhibits low cytotoxicity against human breast cancer MCF-7 cells; at concentrations as high as 1.02 mg mL^-1, the cell survival rate remains >90% after 24 h of incubation^[1].
After conjugation with S2.2 aptamer sodium (0.41 mg/mL; 90 min), SiND-Cy5 enables highly specific targeted fluorescence imaging of MUC1-positive human breast cancer MCF-7 cells, and no binding to MUC1-negative MCF-10A cells or Vero cells is detected^[1].
S2.2 aptamer sodium binds to the VNTR region of TA-MUC1 with high affinity (K_d=0.135 nM or 13.6 nM), and exhibits better specificity than the monoclonal antibody C595 (HY-P990831), including the ability to detect single-mutant epitopes^[3].
Conjugation of S2.2 aptamer sodium with Doxorubicin (HY-15142) enhances cell penetration, promotes Doxorubicin (DOX) release, and reduces the IC₅₀ of DOX in MUC1-positive cancer cells^[3].
S2.2 aptamer sodium-miR-29b chimera restores PTEN expression, induces apoptosis in OVCAR-3 ovarian cancer cells, and sensitizes Paclitaxel (HY-B0015)-resistant OVCAR-3 cells to Paclitaxel (PTX)^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

S2.2 aptamer-miR-29b chimera inhibits tumor growth in ovarian cancer xenograft models, including Paclitaxel (HY-B0015) -resistant tumors, and sensitizes drug-resistant tumors to paclitaxel via the PTEN-Akt-Bax apoptotic pathway and downregulation of oncogenic targets^[3].
S2.2 aptamer sodium-modified nanoliposomes effectively inhibit MCF-7 tumor growth and reduce doxorubicin-induced myocardial cytotoxicity under near-infrared light irradiation^[3].
Polyethylene glycol modification of S2.2 aptamer sodium reduces systemic clearance but impairs tumor uptake in MCF7 xenograft mice^[3].
S2.2 aptamer sodium can target MCF7 xenograft tumors. The tumor uptake of S2.2 aptamer sodium is slightly lower than that of 5TR1 aptamer, and its internalization rate is slower^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

7664.00

Solid

White to off-white

[S2.2 aptamer (sodium)]

Room temperature in continental US; may vary elsewhere.

-20°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

• [1]. Zhang Y, et al. Silicon nanodot-based aptasensor for fluorescence turn-on detection of mucin 1 and targeted cancer cell imaging. Anal Chim Acta. 2018;1035:154-160.  [Content Brief]

  [2]. Zhu Y, et al. Use of S2.2/DOX Magnetic Nanoliposomes in MR Molecule Imaging and Targeted Thermochemotherapy for Breast Cancer In Vitro. Technol Cancer Res Treat. 2023;22:15330338231194498.

  [3]. Nabavinia MS, et al. Anti-MUC1 aptamer: A potential opportunity for cancer treatment. Med Res Rev. 2017;37(6):1518-1539.