Observe MOA in
human tumor tissue
as early as possible

CANscript’s ex vivo human tumor model recapitulates and preserves the native, heterogenous patient-autologous tumor microenvironment (TME), so you can obtain data from real human tumors as early as possible before clinical trials.

Clearly define the underlying biology and modulation of your drug

Accurately understand how your drug affects the tumor microenvironment in humans

Reveal the resistance mechanisms of non-responding patients

Perform repeatable interrogation of mechanism across multiple patient samples in a clinically-representative TME

Develop a solid understanding of MOA prior to human trials

To understand mechanism of action in immuno-oncology research, preservation of the immune compartment, native tumor architecture and specific cells are critical.

CANscript uniquely includes autologous PBMCs with the tumor fragments. This unique culture, alongside observed immune cell modulation such as T-cell infiltration into the tumor during drug interrogation, allows IO researchers to observe mechanism of action in compounds of interest.

Recapitulating the human tumor microenvironment

Advance oncology drug candidates from a pre-clinical setting into the right trial-stage patient population.

CANscript study data uniquely confirms the model captures mechanistic response across many categories of drug mechanisms – including bi-specifics, antibodies, and small molecule compounds – in the ex vivo recapitulated human TME.

  • Relieve checkpoint suppression
  • Direct pro-inflammatory cytokine
  • Relief of metabolic suppression
  • Innate agonism
  • Bacterial toxin delivery
  • Direct T-cell agonism

Identify and observe resistance mechanisms to inform responder populations

Advance oncology drug candidates from a pre-clinical setting into the right trial-stage patient population. 

CANscript provides molecular data and insights on resistance elements to elucidate characteristics of non-response. Get a panel of exploratory assays to construct a customer-relevant view of mechanistic touchstones across multiple patient samples. 

See What Works

Nonuniform T-cell infiltration induced by
PD-1 checkpoint blockade, ex-vivo,
predicts distinct clinical response

See HOW it Works

Mechanistic insights into the role of cAMP-regulated EPAC1 in tumor-induced angiogenesis and metastatic potential in TNBC

Human. Efficient. Multiplexed.

CANscript starts with a tumor sample taken either from a biopsy or surgical resection, and a blood sample from the same donor. The tissue sample is divided into fragments that preserve the heterogeneity of the tumor, including tumor cells, immune cells, and stromal components.

The parallel sections, along with the autologous plasma, are then placed into wells coated with indication and grade-matched matrix proteins, recapitulating the tumor microenvironment.

CANscript employs a series of phenotypic endpoints into an M-score, developed from a machine learning algorithm trained and tested on thousands of patients, providing an accurate prediction of clinical response for each compound of interest.

As a result, multiple therapeutic options can be weighed simultaneously and with a high degree of accuracy, allowing researchers to understand mechanism of action and to prioritize the most promising candidates for advancement into clinical trials.

We’ll work with you every step of the way to increase your chance of clinical trial success so you won’t get lost in translation.