Custom Lentivirus Production Service

Begin your customized Lentivirus production process

Introduction to Pre-made Lentivirus Production Service

Lentivirus is a powerful tool for delivering target genes into almost all types of mammalian cells in vitro and in vivo. In contrast to retroviruses, lentiviruses are imported much more actively into the nuclei of non-dividing cells and are stably integrated into the host cells’ genome independent of cell cycle. Compared to adenovirus and adeno-associated virus (AAV), HIV-based lentiviruses are much less cell toxic, less immunogenicity, and have better transduction efficiency in many cell types, and therefore hold unique promise as gene transfer agents. Genemedi engineered transfer and packaging lentivectors offer the highest lentiviral titers available along with a wide range of selection features including a broad variety of antibiotic selection markers and fluorescent-antibiotic fusion markers for real-time transduction monitoring.

Genemedi launched more than 10 thousand transgene plasmids, which have been sequenced to guarantee the right sequence. These premade plasmid pool are available for direct lentivirus packaging and may greatly shorten the supply period of lentivirus for more than 2 weeks.

Applications for Pre-made Lentivirus:
– Delivery of expression into hard-to-transfect cell types, such as neuronal cells, without using any transfection reagents.
– Highly reproducible and controllable expression delivery method.
– Creation of stable cell lines for long-term, high-level expression.
– Expression of genes in primary or drug-arrested cells.
– Creation of transgenic animals.
– Sub-cellular localization analysis by organelle targeting.


Lentivirus from premade plasmid
Quantity/Unit Vials
Form Frozen form
Suitable Types of Infection In vivo infection in animals
Sipping and Storage Guidelines Shipped by dry ice, stored at -80 ℃, effective for 1 year. Avoid repeatedly freezing and thawing.
Titer > 1*10^8 TU/ml.


1. Provide a ready-to-use, easy delivery method for specific target and shrna expression.

2. Free of the often troublesome lentivector contraction and lentiviral virus production.

3. Consistent and reliable titers delivered at or above specified titer levels.

4. Fast turnaround time.

5. Safe-to-use (self-inactivating) lentiviral particles can deliver your gene into a wide range of cell lines including non-dividing, primary or stem cells.

6. Expert technical support, full confidentiality, and on-time delivery with all projects completed on-site.

Quality control description

Our optimized production of lentiviral vector and strict quality control systems supply customers with a high titer of functional recombinant lentiviral vectors. Two methods are employed to determine viral titers: physical titer (VP/mL) and functional titer (TU/mL). Physical titer is calculated by the level of protein, such as p24, or viral nucleic acid. The functional titer, a calculation of the active virus that can infect cells, is much less than the physical titer (100-1000 fold lower). The method we adopted is functional titer, which is an accurate solution for testing virus accurate activity and MOI. The physical titer can only reflect the number of virus particles, but not reflect the true viral activity, which will cause a large error in subsequent infection experiments.

Technical Documents

1. For further information about lentivirus administration and transduction, please see pdf downloadLentivirus User Manual.


1.Wu, J. et al. MicroRNA-30 family members regulate calcium/calcineurin signaling in podocytes. Journal of Clinical Investigation 125, 4091-4106 (2015).
2.Li, F., Li, S. & Cheng, T. TGF-β1 Promotes Osteosarcoma Cell Migration and Invasion Through the miR- 143-Versican Pathway. Cellular Physiology and Biochemistry 34, 2169-2179 (2014).
3.Liu, Z. et al. miR-451a Inhibited Cell Proliferation and Enhanced Tamoxifen Sensitive in Breast Cancer via Macrophage Migration Inhibitory Factor. BioMed Research International 2015, 207684-207684 (2015).
4.Si, L. et al. Smad4 mediated BMP2 signal is essential for the regulation of GATA4 and Nkx2.5 by affecting the histone H3 acetylation in H9c2 cells. Biochemical and Biophysical Research Communications 450, 81-86 (2014).
5.Han, H., Yang, S., Lin, S. G., Xu, C. S. & Han, Z. Effects and mechanism of downregulation of COX‑2 expression by RNA interference on proliferation and apoptosis of human breast cancer MCF‑7 cells. Molecular Medicine Reports 10, 3092-3098 (2014).
6.Zhang, G., Liu, Z., Cui, G., Wang, X. & Yang, Z. MicroRNA-486-5p targeting PIM-1 suppresses cell proliferation in breast cancer cells. Tumor Biology 35, 11137-11145 (2014).
7.Li, G. et al. CYC1 silencing sensitizes osteosarcoma cells to TRAIL-induced apoptosis. Cellular Physiology and Biochemistry 34, 2070-2080 (2014).
8.Mao, J., Lv, Z. & Zhuang, Y. MicroRNA-23a is involved in tumor necrosis factor-α induced apoptosis in mesenchymal stem cells and myocardial infarction. Experimental and Molecular Pathology 97, 23-30 (2014).
9.Liu, X. et al. Role of human pulmonary fibroblast-derived MCP-1 in cell activation and migration in experimental silicosis. Toxicology and Applied Pharmacology 288, 152-160 (2015).
10.Guan, G. et al. CXCR4-targeted near-infrared imaging allows detection of orthotopic and metastatic human osteosarcoma in a mouse model. Scientific Reports 5, 15244-15244 (2015).
11.Zhang, Y. et al. Role of high-mobility group box 1 in methamphetamine-induced activation and migration of astrocytes. Journal of Neuroinflammation 12, 156-156 (2015).
12.Zhu, T. et al. The Role of MCPIP1 in Ischemia/Reperfusion Injury-Induced HUVEC Migration and Apoptosis. Cellular Physiology and Biochemistry 37, 577-591 (2015).
13.Qian, M. et al. P50-associated COX-2 extragenic RNA (PACER) overexpression promotes proliferation and metastasis of osteosarcoma cells by activating COX-2 gene. Tumor Biology 37, 3879-3886 (2016).
14.Wu, N., Song, Y., Pang, L. & Chen, Z. CRCT1 regulated by microRNA-520 g inhibits proliferation and induces apoptosis in esophageal squamous cell cancer. Tumor Biology 37, 8271-8279 (2016).
15.Wang, Y. et al. Overexpression of Hiwi Inhibits the Growth and Migration of Chronic Myeloid Leukemia Cells. Cell Biochemistry and Biophysics 73, 117-124 (2015).
16.Niu, L. et al. RNF43 Inhibits Cancer Cell Proliferation and Could be a Potential Prognostic Factor for Human Gastric Carcinoma. Cellular Physiology and Biochemistry 36, 1835-1846 (2015).
17.Zhang, H. et al. ZC3H12D attenuated inflammation responses by reducing mRNA stability of proinflammatory genes. Molecular Immunology 67, 206-212 (2015).
18.Deng, X. et al. MiR-146b-5p Promotes Metastasis and Induces Epithelial-Mesenchymal Transition in Thyroid Cancer by Targeting ZNRF3. Cellular Physiology and Biochemistry 35, 71-82 (2015).
19.Zhang, B. et al. HSF1 Relieves Amyloid-β-Induced Cardiomyocytes Apoptosis. Cell Biochemistry and Biophysics 72, 579-587 (2015).
20.Hu, Q. et al. Periostin Mediates TGF-β-Induced Epithelial Mesenchymal Transition in Prostate Cancer Cells. Cellular Physiology and Biochemistry 36, 799-809 (2015).
21.Yang, Z. et al. CD49f Acts as an Inflammation Sensor to Regulate Differentiation, Adhesion, and Migration of Human Mesenchymal Stem Cells. Stem Cells 33, 2798-2810 (2015).
22.Wang, X. et al. MCPIP1 Regulates Alveolar Macrophage Apoptosis and Pulmonary Fibroblast Activation After in vitro Exposure to Silica. Toxicological Sciences 151, 126-138 (2016).
23.Gu, S., Ran, S., Liu, B. & Liang, J. miR-152 induces human dental pulp stem cell senescence by inhibiting SIRT7 expression. FEBS Letters 590, 1123-1131 (2016).
24.Jin, F., Qiao, C., Luan, N. & Li, H. Lentivirus-mediated PHLDA2 overexpression inhibits trophoblast proliferation, migration and invasion, and induces apoptosis. International Journal of Molecular Medicine 37, 949-957 (2016).
25.Liu, Z., Song, Y., Wan, L., Zhang, Y. & Zhou, L. Over-expression of miR-451a can enhance the sensitivity of breast cancer cells to tamoxifen by regulating 14-3-3ζ, estrogen receptor α, and autophagy. Life Sciences 149, 104-113 (2016).
26.Tian, Y. et al. MicroRNA-30a promotes chondrogenic differentiation of mesenchymal stem cells through inhibiting Delta-like 4 expression. Life Sciences 148, 220-228 (2016).
27.Xu, S. et al. MicroRNA-33 promotes the replicative senescence of mouse embryonic fibroblasts by suppressing CDK6. Biochemical and Biophysical Research Communications 473, 1064-1070 (2016).
28.Chen, H., Sun, M., Liu, J., Tong, C. & Meng, T. Silencing of Paternally Expressed Gene 10 Inhibits Trophoblast Proliferation and Invasion. PLOS ONE 10 (2015).
29.Deng, Y. et al. Repair of critical-sized bone defects with anti-miR-31-expressing bone marrow stromal stem cells and poly(glycerol sebacate) scaffolds. European Cells & Materials 27, 13-25 (2014).
30.Zheng, Y. & Xu, Z. MicroRNA-22 induces endothelial progenitor cell senescence by targeting AKT3. Cellular Physiology and Biochemistry 34, 1547-1555 (2014).
31.Yang, X. et al. A lentiviral sponge for miRNA-21 diminishes aerobic glycolysis in bladder cancer T24 cells via the PTEN/PI3K/AKT/mTOR axis. Tumor Biology 36, 383-391 (2015).
32.Wang, W. et al. p53/PUMA expression in human pulmonary fibroblasts mediates cell activation and migration in silicosis. Scientific Reports 5, 16900-16900 (2015).
33.Zhang, S. & Qi, Q. MTSS1 suppresses cell migration and invasion by targeting CTTN in glioblastoma. Journal of Neuro-oncology 121, 425-431 (2015).
34.Wang, P. et al. PFDN1, an indicator for colorectal cancer prognosis, enhances tumor cell proliferation and motility through cytoskeletal reorganization. Medical Oncology 32, 264-264 (2015).
35.Gu, S. et al. Human Dental Pulp Stem Cells via the NF-κB Pathway. Cellular Physiology and Biochemistry 36, 1725-1734 (2015).
36.Huang, G. et al. Clinical and therapeutic significance of sirtuin-4 expression in colorectal cancer. Oncology Reports 35, 2801-2810 (2016).
37.Yan, X., Ye, T., Hu, X., Zhao, P. & Wang, X. 58-F, a flavanone from Ophiopogon japonicus, prevents hepatocyte death by decreasing lysosomal membrane permeability. Scientific Reports 6, 27875 (2016).
38.Ding, W., Tong, Y., Zhang, X., Pan, M. & Chen, S. Study of Arsenic Sulfide in Solid Tumor Cells Reveals Regulation of Nuclear Factors of Activated T-cells by PML and p53. Scientific Reports 6, 19793-19793 (2016).

This site uses cookies to offer you a better browsing experience. By browsing this website, you agree to our use of cookies.