The BiTE® universe
is expanding
with the goal of targeting
multiple tumor types
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Learn how BiTE® molecules are designed to fight cancer
In the body, cancer cells are identified by cytotoxic T cells and eliminated via apoptosis.
However, many cancer cells have developed mechanisms that allow them to evade the immune system, and thus survive and proliferate.
These may include: impaired T cell toxicity, immune suppression, or downregulation of MHC and other factors associated with antigen presentation.
BiTE® immuno-oncology technology is designed to overcome these evasive mechanisms by binding directly to surface antigens on the targeted cancer cell.

BiTE® molecules are designed to engage a patient’s own T cells to directly target cancer cells, with no ex vivo manipulation of the T cells.
BiTE® molecules are engineered from two variable domains: one is specific to CD3 on T cells, the other is specific to a surface antigen highly expressed on the targeted cancer cell.
Half-life extended (HLE) BiTE® molecules contain a fragment-crystallizable (Fc) domain that is designed to extend their time in the body before elimination.
The BiTE® immuno-oncology platform is versatile, allowing for a BiTE® molecule to be engineered to target a tumor-associated antigen across both solid and hematologic malignancies.
Try building a BiTE® molecule that is designed to target this cancer cell.
Build a BiTE® molecule
BiTE® molecule incomplete
Select and drag the domain that is specific to the tumor-associated antigen.
Target:
BCMA
Target:
DLL3
Target:
PSMA
Target:
CD33
Target:
CD19
Target:
CLDN18.2
Target:
FLT3
Target:
MUC17
BiTE® molecule complete
Well done! You’ve successfully built a BiTE® molecule designed to target the tumor-associated antigen CD33. T cells are now able to engage with target cancer cells and may trigger apoptosis.
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Incorrect. This domain targets BCMA.

Find the domain that targets CD33.
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Explore tumor environments
The BiTE® universe is expanding.

The BiTE® immuno-oncology platform offers the versatility to potentially target any tumor-associated antigen across both solid and hematologic malignancies.

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Bone marrow

Multiple myeloma

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Blood vessel

Acute myeloid leukemia

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Prostate acinus

Prostate cancer

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Bronchus

Small-cell lung cancer

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Explore the {{ environment_name }}
{{ factoids_number }} of {{ factoids_number_total }} factoids found
Explore the environment and collect all {{ factoids_number_total }} factoids to release BiTE® molecules.
{{ factoid.title }}
Explore the {{ environment_name }}
{{ factoids_number }} of {{ factoids_number_total }} factoids found
Now that you've finished exploring, release BiTE® molecules to see their potential impact.
Release BiTE® molecules
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Drag the BiTE® molecule that targets {{ env_cancer }} into the environment.
Target:
BCMA
Target:
DLL3
Target:
CD33
Target:
PSMA
Target:
CD19
Target:
CLDN18.2
Target:
FLT3
Target:
MUC17
The versatility of the BiTE® platform allows it to be engineered to target a tumor-associated antigen across both solid and hematologic malignancies.

BiTE® molecule released
Watch the simulation to see the potential impact of BiTE® molecules on the environment.
BiTE® molecule released
Continue exploring the environment to watch BiTE® molecules in action.
BiTE® molecule released
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of BiTE® molecules
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Multiple Myeloma

Multiple myeloma is the second most common hematologic malignancy, characterized by abnormal accumulation of clonal plasma cells in the bone marrow.
Tumor escape mechanisms

Evasive myeloma cells have developed escape mechanisms that allow them to survive, such as immune suppression and downregulation of MHC antigen presentation.
Unmet need

Almost all myeloma patients relapse, and response rates decline with each subsequent line of therapy following relapse.

Successful outcomes are hindered by the complexity of myeloma cell biology, immune suppression, and changes to the bone marrow microenvironment.
Tumor-associated antigen, BCMA

A transmembrane glycoprotein of the TNFR superfamily, BCMA is overexpressed on the myeloma cell membrane of almost all patients with multiple myeloma.

Overexpression of BCMA as well as BCMA ligands, a proliferation-inducing ligand (APRIL) and B cell activating factor (BAFF), enhance proliferation and survival of myeloma cells.
Unmet need

AML is the most common form of acute leukemia in adults, accounting for >250,000 annual deaths worldwide. Average age at diagnosis of AML is 68 years old. The majority of patients with AML will relapse and their survival rate is poor. Overall survival at 5 years is less than 10% in the US elderly population who are older than 65 years of age.

AML has substantial mutation heterogeneity over time, increasing the need for a wide range of treatment options.
Acute myeloid leukemia

AML is a hematologic malignancy characterized by the abnormal growth and differentiation of immature myeloid precursors. Normal myeloid cell production is impeded in AML, resulting in high levels of immature malignant cells and fewer RBCs, platelets, and WBCs.

AML proliferation occurs in the bone marrow, with malignant blast cells migrating to the peripheral blood and other tissue.
Tumor-associated antigen, CD33

CD33 is a transmembrane glycoprotein expressed on the surface of almost all AML blast cells.

At any expression level, CD33 can enable T cell engagement, making it a rational target across a broad set of patients.
Prostate cancer

Prostate cancer remains the #2 cause of cancer-related deaths in men in the US.
Unmet need

Prostate cancer patients are elderly with deteriorating quality of life as a result of disease progression and current treatment side effects.

For over 40 years, hormonal therapy has been the mainstay of prostate cancer treatment. Novel hormonal therapies have improved outcomes for some patients in the metastatic setting but mCRPC remains an incurable disease, representing a major clinical challenge.

Immune-based therapies have had limited effectiveness since prostate cancer is considered an “immunologically cold” tumor with relatively low levels of infiltrating lymphocytes.
Unmet need: NEPC

Neuroendocrine prostate cancer (NEPC) is an aggressive sub-type of prostate cancer that arises from increased use/resistance to novel hormonal therapies; treatment options are limited.
Tumor-associated antigen, PSMA

PSMA is a transmembrane glycoprotein that is expressed in normal prostate tissue and regulates cell growth and survival.
Small-cell lung cancer

Every year, there are ~1.7 million deaths worldwide from all types of lung malignancies, making lung cancer the leading cause of cancer death.

SCLC is a form of neuroendocrine cancer that grows quickly and spreads to other organs.
Unmet need

SCLC accounts for ~15% of all lung cancers, with more than 300,000 new diagnoses worldwide each year.

SCLC is associated with a poor prognosis and a 5-year survival rate of 6%; treatment options are limited.
Tumor-associated antigen, DLL3

DLL3 is a surface antigen that is expressed on the cell surface of SCLC cells and other neuroendocrine tumor cells, with absent or rare expression on non-malignant cells.
{{ environment_name.charAt(0).toUpperCase() + environment_name.slice(1) }}
Myeloma cell
T cell
Osteoclast
Stromal cell
Osteoblast
Plasma cell
Leukemia cell
RBC
Endothelial cell
T cell
Cancerous gland cell
T cell
Neuroendocrine cell
Healthy gland cell
Cancer cell
T cell
Neuroendocrine cell
Goblet cell
Ciliated endothelial cell
BiTE® molecules engage a patient’s existing T cells to directly target cancer cells.
BiTE® molecules can bind to both T cells and myeloma cells, overcoming the tumor’s evasive mechanisms.
Apoptosis of myeloma cell is triggered.
BiTE® molecules engage a patient’s existing T cells to directly target cancer cells.
BiTE® molecules can bind to both T cells and leukemia cells, overcoming the tumor’s evasive mechanisms.
Apoptosis of leukemia cell is triggered.
BiTE® molecules engage a patient’s existing T cells to directly target cancer cells.
BiTE® molecules can bind to both T cells and cancer cells, overcoming the tumor’s evasive mechanisms.
Apoptosis of prostate cancer cell is triggered.
BiTE® molecules engage a patient’s existing T cells to directly target cancer cells.
BiTE® molecules can bind to both T cells and SCLC cells, overcoming the tumor’s evasive mechanisms.
Apoptosis of cancer cell is triggered.
Incorrect. This BiTE® molecule targets PSMA, which is over-expressed in prostate cells.

Find the BiTE® molecule that targets the tumor antigen BCMA.
Try again
BiTE® molecule release successful.

Simulation in progress...
Simulation in progress...
Cancer cell
HLE BiTE® molecule
T cell
BiTE® molecule
T cell
Cancer cell
Cancer cell
HLE BiTE® molecule
T cell
Cancer cell
T cell
HLE BiTE® molecule
Apoptosis triggered
Apoptosis triggered
Apoptosis triggered
Apoptosis triggered
HLE BiTE® molecule
T cell
Myeloma cell
HLE BiTE® molecule
T cell
Apoptosis triggered
BiTE® molecule
T cell
Leukemia cell
BiTE® molecule
T cell
Apoptosis triggered
HLE BiTE® molecule
T cell
Cancer cell
HLE BiTE® molecule
T cell
Apoptosis triggered
HLE BiTE® molecule
T cell
SCLC cell
HLE BiTE® molecule
T cell
Apoptosis triggered
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References
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USA-OCF-81190
References
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