micrOFF™ miRNA antagomir is a specially chemically modified miRNA antagonist that binds to mature miRNAs in vivo to prevent complementary pairing of miRNAs with their target mRNAs and inhibits miRNA activity. The miRNA antagomir is a reverse complement of the mature strand of miRNA. The entire strand is methylated and has 2 and 4 base thio modifications at the 5′ and 3′ ends, respectively. A high affinity cholesterol modification is attached to the 3′ end. Compared with common inhibitors, micrOFF miRNA antagomir has higher stability and inhibition in animal experiments and cell experiments, and is more easily enriched in target cells through cell membranes and tissue gaps.
The transfection efficiency of miRNA antagomir is higher in cell experiments and does not require transfection reagents, thus avoiding the complex steps of the transfection reagent packaging process and its impact on the experiment. It can be administered in animal experiments by systemic or local injection, and the effect can last for weeks.
1. Low toxicity, world-leading proprietary technology
2. Chemically modified, can be directly injected into animals, no transfection reagent needed
3. Shorter synthesis cycle compared with viral vector, convenient for the subsequent development of Oligonucleotide-based drugs in transformation medicine 4. Highly stable, easy to penetrate cell membranes and tissue gaps.
Which RNAi Control is right for you？
Refer to the table below to pick the right RNAi control for your research:
Injecting miRNA-328 antagomir to WT and TG mice through the tail vein for 3 days at a dose of 80 mg/kg, and the detection was conducted 4 weeks later. The results showed that elevated miRNA-328 can induce arrhythmias, and that miRNA-328 regulates CACNA1C protein in calcium channels.( Lu Y, et al. Circulation, 2010.)
The high expression of miR-151 significantly increased the migration, invasion and metastasis of hepatoma cells. antagomir was applied to inhibit the high expression of miRNA, so as to further inhibit tumor cell metastasis. (Ding J, et al. Nat Cell Biol, 2010.)
After injecting antagomir-276 into aphids, the hatching rate and embryonic stage distribution changed. (He J, et al. Proc Natl Acad Sci USA. 2016.)
|miR30000527-4-5||micrOFF mmu-miR-16-5p antagomir,in vivo,5nmol||mouse||$199.92|
|miR30000830-4-5||micrOFF rno-miR-125b-5p antagomir,in vivo,5nmol||rat||$199.92|
|miR30000530-4-5||micrOFF mmu-miR-21a-5p antagomir,in vivo,5nmol||mouse||$199.92|
|miR30000537-4-5||micrOFF mmu-miR-27a-3p antagomir,in vivo,5nmol||mouse||$199.92|
|miR30000123-4-5||micrOFF mmu-miR-1a-3p antagomir,in vivo,5nmol||mouse||$199.92|
|miR30000584-4-5||micrOFF mmu-miR-339-5p antagomir,in vivo,5nmol||mouse||$199.92|
|miR30000159-4-5||micrOFF mmu-miR-149-5p antagomir,in vivo,5nmol||mouse||$199.92|
|miR30000677-4-5||micrOFF mmu-miR-7a-5p antagomir,in vivo,5nmol||mouse||$199.92|
|miR30004853-4-5||micrOFF mmu-miR-874-3p antagomir,in vivo,5nmol||mouse||$199.92|
|miR30000383-4-5||micrOFF mmu-let-7d-5p antagomir,in vivo,5nmol||mouse||$199.92|
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