pd-1/pd-l1

PD-1/PD-L1 inhibitory peptide C8 disrupts the PD-1/PD-L1 interaction, leading to the activation of CD8+ and CD4+ T cells and an increase in IFN-γ secretion. In mouse models, PD-1/PD-L1 inhibitory peptide C8 has demonstrated antitumor activity.

BMSpep-57 hydrochloride, a potent macrocyclic peptide, competitively inhibits PD-1/PD-L1 interaction, exhibiting an IC50 value of 7.68 nM. It binds to PD-L1 with dissociation constants (Kds) of 19 nM and 19.88 nM as determined by MST and SPR assays, respectively. This compound enhances T cell functionality by promoting IL-2 production in PBMCs[1].

BMSpep-57, a potent macrocyclic peptide inhibitor, competitively disrupts the PD-1/PD-L1 interaction, demonstrating a significant inhibitory concentration (IC50) of 7.68 nM. It exhibits binding affinity towards PD-L1 with dissociation constants (Kd) of 19 nM and 19.88 nM in MicroScale Thermophoresis (MST) and Surface Plasmon Resonance (SPR) assays, respectively. This compound enhances T cell functionality by promoting Interleukin-2 (IL-2) production within Peripheral Blood Mononuclear Cells (PBMCs).

Human PD-L1 inhibitor IV is a polypeptide compound that competitively inhibits the human PD-1 protein. It has a Kd value of 1.38 μM and effectively blocks the interaction between hPD-1 and hPD-L1.

Human PD-L1 inhibitor III [Human PD-L1 inhibitor] is a bioactive compound designed to inhibit the programmed death-ligand 1 (PD-L1) protein in humans.

Human PD-L1 inhibitor II, a potent PD-L1 inhibitor, exhibits strong anti-cancer activity.

Human PD-L1 inhibitor I is a peptide ligand that specifically inhibits the interaction between human PD-L1 and human PD-1, exhibiting a KD value of 3.39 μM, indicating its binding affinity. The presence of Human PD-L1 inhibitor I disrupts their binding, thereby attenuating their respective functions.

[D-Leu-4]-OB3 suppresses the expression of genes associated with inflammation, proliferation, and metastasis, as well as the expression of PD-L1. Additionally, it promotes the expression of genes that induce apoptosis [1].

Human PD-L1 Inhibitor V is a peptide that binds to the human PD-1 protein with an affinity characterized by a dissociation constant (Kd) of 3.32 μM, effectively inhibiting the hPD-1/hPD-L1 interaction [1].

Human PD-L1 Inhibitor V TFA, a peptide that binds to the human PD-1 protein, exhibits a dissociation constant (Kd) of 3.32 μM and effectively inhibits the hPD-1/hPD-L1 interaction [1].

TPP-1, a potent inhibitor of the PD-1/PD-L1 interaction, exhibits high affinity for PD-L1, with a dissociation constant (K D) of 95 nM. It effectively inhibits human tumor growth in vivo by reactivating T-cell function [1].

TPP-1 TFA, a potent inhibitor of the PD-1/PD-L1 interaction, selectively binds to PD-L1 with high affinity (K D =95 nM). It effectively inhibits human tumor growth in vivo by reactivating T-cell function [1].

WL12 is a peptide that targets and binds specifically to programmed death ligand 1 (PD-L1). It can be radiolabeled with various radionuclides to produce radiotracers, enabling the evaluation of PD-L1 expression in tumors [1].

(D)-PPA 1 TFA, a hydrolysis-resistant D-peptide antagonist, is a potent PD-1/PD-L1 inhibitor with an affinity for PD-1 of 0.51 μM, demonstrating efficacy both in vitro and in vivo [1].

Human membrane-bound PD-L1 polypeptide serves as an antigen for inducing the production of PD-L1 antibodies [1].

Sotiburafusp alfa is a humanized bispecific fusion protein comprising a VEGFR-1 extracellular domain fragment (129-228, 1-100 in the current sequence) connected through a 101 GGSGGSGGSGGSGGS 115 peptide linker to the N-terminus (116-564) of a humanized IgG1-kappa anti-human PD-L1 heavy chain with L352>A and L353>A mutations. Additionally, sotiburafusp alfa functions as an angiogenesis inhibitor [1].

Eciskafusp alfa, a cis-targeted IL2v immunocytokine, acts on programmed cell death 1 (PDCD1, commonly known as PD-1), preferentially targeting antigen-specific stem-like PD-1+ TCF-1+ CD8+ T cells to differentiate into a more effective effector population. This compound is applicable in the study of cancer and chronic infections [1].

AUNP-12 acetate is a polypeptide inhibitor of PD-1 that is equivalent to PD-1 and PD-2 in inhibiting lymphocyte proliferation and effector fuction, in addition to immune activation and antitumor activity.

PL120131 is a PD-1/PD-L1 inhibitory peptide that disrupts the interaction between PD-1 and PD-L1 by binding to PD-1. This compound can inhibit the apoptosis signaling pathway mediated by PD-1, thereby preventing apoptosis (apoptosis) in Jurkat cells and primary lymphocytes. Additionally, PL120131 supports cytotoxic T lymphocytes (CTL) in exhibiting antitumor activity.

PD-L1 inhibitory peptide TFA is an inhibitory peptide targeting programmed cell death ligand 1 (PD-L1). It binds to PD-L1, lifting immune suppression and restoring the antitumor activity of T cells. PD-L1 inhibitory peptide TFA shows potential for use in cancer research.

Cilengitide (EMD 121974) is a potent integrin inhibitor for the αvβ3/5 receptor (IC50: 4.1/79 nM, in cell-free assays) with approximately 10-fold selectivity against gpIIbIIIa.

AUNP-12, a new immune checkpoint modulator, is an inhibitor of the PD-1 pathway.

H-20 is a PD-1 agonist that reduces the required dosage of morphine for analgesia. It can be used in studies related to chronic pain.

RK-10 is a peptide that binds to PD-L1. After being conjugated with Cy5 or Biotin, RK-10 can be used to identify PD-L1-expressing tumors through flow cytometry or immunohistochemistry. It is applicable for research in detecting cancers such as non-small cell lung cancer (NSCLC), breast cancer, squamous cell carcinoma, and melanoma.