Lentivirus

The anti-CD20 CAR lentiviruses are replication incompetent, HIV-based, VSV-G-pseudotyped lentiviral particles that are ready to infect almost all types of mammalian cells, including primary and non-dividing cells. These viruses transduce the ScFv (single-chain variable fragment) of anti-CD20 (clone Leu-16) linked to a 2^nd generation CAR (Chimeric Antigen Receptor) containing CD8 hinge and transmembrane domains, and the 4-1BB and CD3ζ signaling domains .

The anti-CD22 CAR lentiviruses are replication incompetent, HIV-based, VSV-G-pseudotyped lentiviral particles that are ready to infect almost all types of mammalian cells, including primary and non-dividing cells. These viruses transduce the ScFv (single-chain variable fragment) of anti-CD22 (clone m971) linked to a 2^nd generation CAR (Chimeric Antigen Receptor) containing CD8 hinge and transmembrane domains, and the 4-1BB and CD3ζ signaling domains (below).

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. Numerous SARS-CoV-2 variants have been identified so far. These variants contain a number of mutations that may increase morbidity and mortality and allow the virus to spread more easily and quickly than the original strain. BPS Bioscience has launched a series of Spike Variants (SARS-CoV-2) Pseudotyped Lentivirus (Luc reporter). The Spike (SARS-CoV-2) Pseudotyped Lentiviruses were produced with SARS-CoV-2 S

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 ACE2 may offer protection against the viral infection. A variant called B.1.621 (also known as the Mu Variant) was first identified in Columbia in early 2021. This variant has a number of mutations that may increase morbidity and mortality and allow the virus to spread more easily and quickly than other variants. The Spike (B.1.621, Mu Variant) (SARS-CoV-2) Pseudotyped Lentiviruses were produced with SARS-CoV-2 B.1.621 Variant Spike (Genbank Accession #QHD43416.1 with

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 ACE2 may offer protection against the viral infection. A variant called B.1.621 (also known as the Mu Variant) was first identified in Columbia in early 2021. This variant has a number of mutations that may increase morbidity and mortality and allow the virus to spread more easily and quickly than other variants. The Spike (B.1.621, Mu Variant) (SARS-CoV-2) Pseudotyped Lentiviruses were produced with SARS-CoV-2 B.1.621 Variant Spike (Genbank Accession #QHD43416.1 with

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 ACE2 may offer protection against the viral infection. A variant called B.1.1.529 BA.1 (also known as the 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. A sub-lineage of BA.1 with an R346K substitution in the spike protein is classified as B.1.1.529 BA.1.1. The Spike (B.1.1.529 BA.1.1, Omicron Variant R346K) (SARS-CoV-2) Pseudo

Please note this product may be subject to fees, we invite you to contact your local office. The UAS (Upstream Activation Sequence) Luciferase Reporter Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to transduce almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a firefly luciferase gene driven by a multimerized GAL4 upstream activation sequence (UAS) located upstream of the minimal TATA promoter and an antibiotic selection gene (puromycin) for the selection of stable clones. After transduction, the UAS-controlled signaling pathway in the target cells can be monitored by measuring the luciferase activity.

Please note this product may be subject to fees, we invite you to contact your local office. GAL4 DBD-GR (GAL4 DNA binding domain-glucocorticoid receptor) lentivirus are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to transduce almost all types of mammalian cells, including primary and non-dividing cells. The particles express a fusion protein in which the glucocorticoid receptor (GR) ligand binding domain is fused to the DNA binding domain of GAL4 (GAL4 DBD).  After co-transduction of GAL4 DBD-GR lentivirus and GAL4-responsive UAS luciferase reporter lentivirus (BPS Bioscience #78631), the glucocorticoid-induced activation of the glucocorticoid receptor can be monitored by measuring the luciferase activity.

Please note this product may be subject to fees, we invite you to contact your local office. CD8 (cluster of differentiation 8) is a cell surface glycoprotein found on most cytotoxic T lymphocytes that functions within the immune system to mediate cell-cell interactions. The functional forms of CD8 consist of either a heterodimer of two isoforms, CD8α and CD8β, or a homodimer of two CD8α molecules. CD8 acts as a coreceptor to facilitate binding between the T-cell Receptor (TCR) and the class I Major Histocompatibility Complex (MHC).  Studying CD8 and its importance in isoimmunity can further our understanding of post-transplant recognition. The CD8a (CD8α, CD8 alpha) 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 CD8a (NM_001768.6) driven by an EF1a promoter and a puromycin selection marker.)