Pipeline

By leveraging our deep expertise in protein drug discovery, our immunotherapy pipeline has been specifically curated to target clinically validated as well as emerging mechanisms, positioning our portfolio to pursue both best-in-class and first-in-class approaches.

ProgramMechanism of ActionLead IDLead OPIND EnablingClinic
BPT567
(PD1-IL18)
Immuno-oncology
 PD-1 blockade
+ tumor targeting
+ IL-18 signaling
IL-18 binding protein resistant

 

IL-18 is a strong stimulator of both innate and adaptive immunity, which makes it a potent and attractive therapeutic candidate for cancer immunotherapy. Native IL-18 cytokine activates the IL-18 receptor to induce proinflammatory effects including potent induction of IFNγ, but also binds to a negative feedback inhibitor, IL-18 Binding Protein (IL-18BP). IL-18BP is frequently upregulated and abundant in the tumor microenvironment and is also induced by IFNγ in a natural negative feedback loop. In patients, IL-18BP binds native IL-18 and blocks the cytokine from activating its receptor, leading to a ‘quenching’ effect and ultimately tachyphylaxis.

Bright Peak’s enhanced IL-18 cytokine payload is specifically engineered to preferentially activate the IL-18 receptor without binding to IL-18BP – triggering potent pro-inflammatory signaling in antitumor immune cells without being neutralized by IL-18BP.

PD1-IL18 consists of Bright Peak’s enhanced IL-18 payload chemically conjugated to LZM009, an anti-PD-1 antibody now in late-stage clinical development. PD1-IL18 targets PD-1+ (antigen-experienced) T cells in the tumor and simultaneously blocks PD-1 while stimulating the IL-18 receptor on the surface of same PD-1+ T cell (cis-signaling) to generate synergistic anti-tumor efficacy.

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BPT331
(PD1-IL2)
Immuno-oncology
 PD-1 blockade
+ tumor targeting
+ β/γ-selective IL-2 signaling
α-dead β-enhanced

 

PD1-IL2 consists of Bright Peak’s enhanced IL-2 payload chemically conjugated to LZM009, an anti-PD-1 antibody now in late-stage clinical development. IL-2 is a master immune-stimulating cytokine with proven efficacy in patients with cancer. PD1-IL2 is designed to target and block PD-1 and simultaneously bind the IL-2 receptor on the surface of the same PD-1+ antigen-experienced T cell (cis-signaling) to generate synergistic anti-tumor efficacy.
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BPT331CAPS
(PD1-IL2CAPS)
Immuno-oncology
 PD-1 blockade
+ tumor-selective activation
+ β/ γ-selective IL-2 signaling
α-dead β-enhanced
Conditionally activated

 

PD1-IL2CAPS consists of Bright Peak’s enhanced IL-2 payload chemically conjugated to LZM009, an anti-PD-1 antibody now in late-stage clinical development, with an additional moiety that enables the IL-2 payload to be conditionally activated when encountering the tumor microenvironment (conditionally activated protein structure or "CAPS") for a potentially expanded therapeutic window and greater safety margin.
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BPT264
(PEG-IL2 AID)
Autoimmune diseases
 α-selective IL-2 signaling
α-enhanced β-dead
Treg enhancer

 

The IL-2 cytokine is a growth factor that is critical for the proliferation all T cells. At low concentrations, it is a known activator and expander of regulatory T cells (Tregs), which in turn can regulate immune responses and attenuate autoimmunity. Tregs have been shown to play a key role in autoimmunity and their expansion using low-dose IL-2 has demonstrated promising preliminary clinical efficacy in autoimmune diseases.

Bright Peak has engineered an enhanced IL-2 cytokine harboring specific modifications to amino acid side chains to uniquely block binding to IL2Rβ and simultaneously enhance binding to IL2Rα, creating an IL-2 mutein that preferentially expands and activates Tregs.

Bright Peak’s IL-2 autoimmune cytokine payload can also be conjugated to antibodies as part of our Immunocytokine platform.

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BPT543
(PEG-IL18)
Immuno-oncology
 IL-18 signaling
IL-18 binding protein resistant

 

Bright Peak’s enhanced IL-18 cytokine payload is specifically engineered to preferentially activate the IL-18 receptor without binding to IL-18BP – triggering potent pro-inflammatory signaling in antitumor immune cells without being neutralized by IL-18BP.

PEG-IL18 consists of Bright Peak’s enhanced IL-18 payload conjugated to PEG to generate a half-life extended molecule for improved pharmacokinetics and convenient administration.
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DrugPhase
BPT567
(PD1-IL18)
Immuno-oncology
Lead OP
BPT331
(PD1-IL2)
Immuno-oncology
Lead OP
BPT331CAPS
(PD1-IL2CAPS)
Immuno-oncology
Lead ID
BPT264
(PEG-IL2 AID)
Autoimmune diseases
Lead OP
BPT543
(PEG-IL18)
Immuno-oncology
Lead OP

BPT567
(PD1-IL18)

IL-18 is a strong stimulator of both innate and adaptive immunity, which makes it a potent and attractive therapeutic candidate for cancer immunotherapy. Native IL-18 cytokine activates the IL-18 receptor to induce proinflammatory effects including potent induction of IFNγ, but also binds to a negative feedback inhibitor, IL-18 Binding Protein (IL-18BP). IL-18BP is frequently upregulated and abundant in the tumor microenvironment and is also induced by IFNγ in a natural negative feedback loop. In patients, IL-18BP binds native IL-18 and blocks the cytokine from activating its receptor, leading to a ‘quenching’ effect and ultimately tachyphylaxis.

Bright Peak’s enhanced IL-18 cytokine payload is specifically engineered to preferentially activate the IL-18 receptor without binding to IL-18BP – triggering potent pro-inflammatory signaling in antitumor immune cells without being neutralized by IL-18BP.

PD1-IL18 consists of Bright Peak’s enhanced IL-18 payload chemically conjugated to LZM009, an anti-PD-1 antibody now in late-stage clinical development. PD1-IL18 targets PD-1+ (antigen-experienced) T cells in the tumor and simultaneously blocks PD-1 while stimulating the IL-18 receptor on the surface of same PD-1+ T cell (cis-signaling) to generate synergistic anti-tumor efficacy.

BPT331
(PD1-IL2)

PD1-IL2 consists of Bright Peak’s enhanced IL-2 payload chemically conjugated to LZM009, an anti-PD-1 antibody now in late-stage clinical development. IL-2 is a master immune-stimulating cytokine with proven efficacy in patients with cancer. PD1-IL2 is designed to target and block PD-1 and simultaneously bind the IL-2 receptor on the surface of the same PD-1+ antigen-experienced T cell (cis-signaling) to generate synergistic anti-tumor efficacy.

BPT331CAPS
(PD1-IL2CAPS)

PD1-IL2CAPS consists of Bright Peak’s enhanced IL-2 payload chemically conjugated to LZM009, an anti-PD-1 antibody now in late-stage clinical development, with an additional moiety that enables the IL-2 payload to be conditionally activated when encountering the tumor microenvironment (conditionally activated protein structure or "CAPS") for a potentially expanded therapeutic window and greater safety margin.

BPT264
(PEG-IL2 AID)

The IL-2 cytokine is a growth factor that is critical for the proliferation all T cells. At low concentrations, it is a known activator and expander of regulatory T cells (Tregs), which in turn can regulate immune responses and attenuate autoimmunity. Tregs have been shown to play a key role in autoimmunity and their expansion using low-dose IL-2 has demonstrated promising preliminary clinical efficacy in autoimmune diseases.

Bright Peak has engineered an enhanced IL-2 cytokine harboring specific modifications to amino acid side chains to uniquely block binding to IL2Rβ and simultaneously enhance binding to IL2Rα, creating an IL-2 mutein that preferentially expands and activates Tregs.

Bright Peak’s IL-2 autoimmune cytokine payload can also be conjugated to antibodies as part of our Immunocytokine platform.

BPT543
(PEG-IL18)

Bright Peak’s enhanced IL-18 cytokine payload is specifically engineered to preferentially activate the IL-18 receptor without binding to IL-18BP – triggering potent pro-inflammatory signaling in antitumor immune cells without being neutralized by IL-18BP.

PEG-IL18 consists of Bright Peak’s enhanced IL-18 payload conjugated to PEG to generate a half-life extended molecule for improved pharmacokinetics and convenient administration.

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