Program | Mechanism of Action | Lead ID | Lead OP | IND Enabling | Clinic | |
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BPT567 (PD1-IL18) Immuno-oncology |
PD-1 blockade + tumor targeting + IL-18 signaling IL-18 binding protein resistant |
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BPT331 (PD1-IL2) Immuno-oncology |
PD-1 blockade + tumor targeting + β/γ-selective IL-2 signaling α-dead β-enhanced |
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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 |
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BPT264 (PEG-IL2 AID) Autoimmune diseases |
α-selective IL-2 signaling α-enhanced β-dead Treg enhancer |
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BPT543 (PEG-IL18) Immuno-oncology |
IL-18 signaling IL-18 binding protein resistant |
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Drug | Phase | BPT567 (PD1-IL18) Immuno-oncology | Lead OP |
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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.