Viral Vectors & Particles

Please note this product may be subject to fees, we invite you to contact your local office. The NKp46 Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to transduce nearly all types of mammalian cells, including primary and non-dividing cells. The particles contain a human NKp46 (NM_004829.7) driven by an EF1A promoter and a puromycin selection marker (Figure 1). <img style="display: block; margin-left: auto; margin-right: auto;" src="{{media url="wysiwyg/Lentivirus/78717.png"}}" alt="" width="391" height="353" /> Figure 1: Schematic of the lenti-vector used to generate the NKp46 Lentivirus.

Please note this product may be subject to fees, we invite you to contact your local office. The EpCAM Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to transduce nearly all types of mammalian cells, including primary and non-dividing cells. The particles contain a human EpCAM (NM_002354.3) driven by an EF1A promoter and a puromycin selection marker (Figure 1). <img src="{{media url="wysiwyg/Lentivirus/78718.png"}}" alt="" width="446" height="363" /> Figure 1: Schematic of the lenti-vector used to generate the EpCAM Lentivirus

The CEACAM5 Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to transduce nearly all types of mammalian cells, including primary and non-dividing cells. The particles contain a human CEACAM5 (NM_004363.6) driven by an EF1A promoter and a puromycin selection marker (Figure 1). <img src="{{media url="wysiwyg/Imtx/78719.png"}}" alt="" width="348" height="310" /> Figure 1: Schematic of the lenti-vector used to generate the CEACAM5 Lentivirus

The CEACAM6 Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to transduce nearly all types of mammalian cells, including primary and non-dividing cells. The particles contain a human CEACAM6 (NM_002483.7) driven by an EF1A promoter and a puromycin selection marker (Figure 1). <img style="display: block; margin-left: auto; margin-right: auto;" src="{{media url="wysiwyg/Imtx/78720.png"}}" alt="" width="426" height="347" /> Figure 1: Schematic of the lenti-vector used to generate the CEACAM6 Lentivirus

Please note this product may be subject to fees, we invite you to contact your local office. The LYPD1 Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to transduce nearly all types of mammalian cells, including primary and non-dividing cells. The particles contain a human LYPD1 (NM_ 001321234.2) driven by a EF1A promoter and a puromycin selection marker (Figure 1). <img style="display: block; margin-left: auto; margin-right: auto;" src="{{media url="wysiwyg/Lentivirus/78724.png"}}" alt="" width="450" height="364" /> Figure 1: Schematic of the lenti-vector used to generate the LYPD1 Lentivirus

The PSMA Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to transduce nearly all types of mammalian cells, including primary and non-dividing cells. The particles contain a human PSMA (NM_ 004476.3) driven by a CMV promoter and a puromycin selection marker (Figure 1). <img src="{{media url="wysiwyg/Imtx/78726.png"}}" alt="" width="352" height="313" /> Figure 1: Schematic of the lenti-vector used to generate the PSMA Lentivirus.

The B7-H4 Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to transduce nearly all types of mammalian cells, including primary and non-dividing cells. The particles contain a human B7-H4 (NM_ 024626.4) driven by a CMV promoter and a puromycin selection marker (Figure 1). <img style="display: block; margin-left: auto; margin-right: auto;" src="{{media url="wysiwyg/Imtx/78727.png"}}" alt="" width="406" height="361" /> Figure 1: Schematic of the lenti-vector used to generate the B7-H4 Lentivirus.

The pandemic coronavirus disease 2019 (COVID-19) is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). As the first step of the viral replication, the virus attaches to the host cell surface before entering the cell. The viral Spike protein recognizes and attaches to the Angiotensin-Converting Enzyme 2 (ACE2) receptor found on the surface of type I and II pneumocytes, endothelial cells, and ciliated bronchial epithelial cells. Drugs targeting the interaction between the Spike protein of SARS-CoV-2 and human ACE2 may offer protection against the viral infection. Omicron Variant was identified in South Africa in November of 2021. This variant has a large number of mutations that allow the virus to spread more easily and quickly than other variants. As of May 2022, Omicron variants were divided into seven distinct sub-lineages: BA.1, BA.1.1, BA.2, BA.3, BA.2.12.1, BA.4, and BA.5. As of January 2023, additional new sub-lineages (e.g. BQ.1, BQ.1.1, BF.7, XBB.1, XBB.1.5)

The pandemic coronavirus disease 2019 (COVID-19) is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). As the first step of the viral replication, the virus attaches to the host cell surface before entering the cell. The viral Spike protein recognizes and attaches to the Angiotensin-Converting Enzyme 2 (ACE2) receptor found on the surface of type I and II pneumocytes, endothelial cells, and ciliated bronchial epithelial cells. Drugs targeting the interaction between the Spike protein of SARS-CoV-2 and human ACE2 may offer protection against the viral infection. Omicron Variant was identified in South Africa in November of 2021. This variant has a large number of mutations that allow the virus to spread more easily and quickly than other variants. As of May 2022, Omicron variants were divided into seven distinct sub-lineages: BA.1, BA.1.1, BA.2, BA.3, BA.2.12.1, BA.4, and BA.5. As of January 2023, additional new sub-lineages (e.g. BQ.1, BQ.1.1, BF.7, XBB.1, XBB.1.5)