Advantages of CYN-101

  • Cancer Targeting: Specifically Targets Cancer Cells via Laminin Receptor
  • Naturally Apoptotic: Kills Targeted Cancer Cells Without Affecting Normal Cells
  • Non Immunogenic: No Neutralizing Antibody Effects Seen to Date
  • Replication Defective: Engineered to Infect Only Once
  • RNA Genome: No Insertion in Host Genome — No Mutagenesis
  • Payload Delivery: Can be Engineered to Include Therapeutic Payload
  • Represents a potential off-the-shelf treatment that requires no special patient specific manufacturing

The Company believes that the Sindbis viral vector technology represents a differentiated and potentially transformational approach for treating solid tumors. Several obstacles (unsuccessfully faced by others) have been overcome that may make this a commercially viable system and the system of choice particularly for metastatic and primary cancer. Below are some of the major advantages and obstacles that have been overcome in part or whole.


The Sindbis viral vectors were originally derived from Sindbis Virus, an alpha virus (RNA genome). Both the wild-type and the engineered vector are naturally transmitted in blood and have long half-lives, which enable intravenous administration.

CYN-101 is similar to the wild-type virus except that it has been rendered replication defective. Once it infects a cell the RNA will code for protein products that trigger apoptosis (programmed cell-death).

Systemic Delivery

The wild-type virus is naturally transmitted in blood and can survive in the blood stream. This makes it a candidate for systemic injection. There is an advantage over other vectors that are lysed in plasma such as lentiviral systems.


Sindbis virus naturally binds to the high affinity laminin receptor (LAMR). While the LAMR is expressed by nearly every mammalian cell, it is over-expressed in many solid tumors. In normal cells, the LAMRs are occupied by laminin, thereby blocking binding by the vector. When LAMR is over-expressed in cancer, the binding sites become available for very specific binding and infection by the vector only to cancer cells. Additionally, Sindbis viral vectors transit through the lymph nodes where they also activate and recruit an immune response to trigger cell death through production of activated CD8+ (or cytotoxic) T cells which migrate to the tumor site and kill tumor bearing tumor associated antigens carried and expressed by the Sindbis virus vectors.

The NYU patents licensed to Cynvec also cover certain methods of custom targeting including the use of tumor associated antigens engineered to be expressed by the Sindbis viral vector to enhance targeting specific cancers. CYN-101, Cynvec’s initial vaccine employs the tumor specific antigen NY-ESO-1 for such targeting.

Little to No Immunogenicity

The wild-type Sindbis virus from which CYN-101 is derived can be associated with a low-level immune response, typically a rash or low-grade fever which usually self-resolve. Immune risk may be further reduced by the controlled dosing at pre-determined titers of replication defective vectors that reduce the possibility of “viremia.”

Apoptotic Characteristic

The vector is naturally apoptotic, enabling its use as a cancer therapeutic (cytoxic) even without a tumor associated antigen, as has been demonstrated in animal experiments.

RNA Vector

The Sinbis genome is RNA, which is not incorporated in the host DNA. There is little to no risk of insertional mutagenesis.

Vector is Replication Defective in Host Cells

CYN-101 is engineered to be replication defective. This may confer it with both therapeutic and regulatory advantages.


CYN-101 is manufactured by transfection of the vector RNA into mammalian cells and purified via column chromatography. Scalable manufacturing methods have been developed, and are currently being optimized to produce therapeutically relevant titers in sufficient quantities for clinical trials.

Back to top

Sindbis Virus