Human OX40 Ligand / TNFSF4 Protein
- Known as:
- Human OX40 Ligand / TNFSF4 Protein
- Catalog number:
- OXL-H52Q8
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human OX40 Ligand / TNFSF4 Protein
Related genes to: Human OX40 Ligand / TNFSF4 Protein
- Gene:
- TNFRSF4 NIH gene
- Name:
- TNF receptor superfamily member 4
- Previous symbol:
- TXGP1L
- Synonyms:
- ACT35, OX40, CD134
- Chromosome:
- 1p36.33
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-15
- Date modifiied:
- 2019-04-23
- Gene:
- TNFSF4 NIH gene
- Name:
- TNF superfamily member 4
- Previous symbol:
- TXGP1
- Synonyms:
- OX-40L, gp34, CD252
- Chromosome:
- 1q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-15
- Date modifiied:
- 2017-03-02
Related products to: Human OX40 Ligand / TNFSF4 Protein
Related articles to: Human OX40 Ligand / TNFSF4 Protein
- The OX40/OX40L axis entered clinical development in atopic dermatitis with a strong biological rationale and early signs of durable activity. However, as the treatment landscape evolved, questions emerged about whether the magnitude of monotherapy benefit was sufficient relative to established and emerging therapies. The discontinuation of rocatinlimab after confirmed and suspected cutaneous Kaposi's sarcoma cases, together with two cumulative cases reported in the amlitelimab program in patients with known risk factors, has changed the discussion from early promise to mechanism, risk, and therapeutic strategy. Although a causal link between OX40/OX40L modulation and Kaposi's sarcoma remains unproven, available human genetic and experimental observations make the association biologically plausible but mechanistically unresolved. The central challenge is now to determine how the axis can be targeted, in which patients, and in what therapeutic context, to maximize clinical benefit while managing risk. Rather than signaling the end of the axis in atopic dermatitis, Kaposi's sarcoma may instead mark the limits of a first-generation development strategy and the beginning of a more selective approach built around molecule design, therapeutic context, and prospective risk mitigation. - Source: PubMed
Publication date: 2026/06/02
Salek-Ardakani Shahram - Clinical trials using monoclonal antibodies targeting the OX40/OX40L axis (AMG451, GBR830, KHK4083, and KY1005) have shown promise in long-term disease modification of atopic dermatitis (AD). OX40/OX40L enhances survival of effector T cells and inhibits regulatory T cells (Tregs) function in other inflammatory diseases, but its mechanism of action in AD is unelucidated. We aimed to evaluate OX40- and OX40L-expressing cells in the skin and blood of AD patients to understand how the axis promotes T cell activity and inflammation. - Source: PubMed
Publication date: 2026/03/07
Yamamura KazuhikoDahabreh DanteDel Duca EsterLozano-Ojalvo DanielKim MadelineMurai-Yamamura MikaGarcet SandraGonzalez JuanaMiura ShunsukeWilliams Samuel CHur Hong BeomLi XuanLiu YingLin Xinyi EMetukuru RagasrutiZhou JerryEstrada Yeriel DKrueger James GGuttman-Yassky Emma - Immunotherapy targeting immune checkpoint proteins (ICPs) has transformed cancer care, yet current treatments focus on a narrow set of inhibitory ICPs and benefit only a subset of patients. The co-stimulatory pair OX40-OX40L, implicated in inflammation and autoimmunity, also plays roles in cancer immunity. We previously showed that high OX40L mRNA expression in melanoma correlates with favorable prognosis and improved responses to PD-1 blockade. However, the protein-level expression and functions of OX40L in melanoma remain poorly defined. - Source: PubMed
Publication date: 2026/01/23
Feldman SusannaDa'ana BaseemOfek NonaElkis LilianaPollak-Moseri AdiRiklin-Nahmias EmmanuelaMendlovic SoniaAvraham AyeletLeibowitz Raya - Atopic dermatitis is a chronic inflammatory skin disorder that affects over 200 million people worldwide. Although disease etiology is multifaceted, the immune checkpoint molecules OX40 and OX40L have a critical role in disease development. Recent clinical trials demonstrated that the OX40-targeting antibodies rocatinlimab (KHK4083/AMG-451) and telazorlimab (GBR-830/ISB-830) and the OX40L-targeting antibody amlitelimab (KY1005) significantly improve symptoms of atopic dermatitis. However, the epitopes where these antibodies bind OX40 and OX40L remain unclear, and therefore, so do the mechanisms through which they specifically disrupt OX40-OX40L signaling. To address this, computational modeling was performed to predict antibody-protein cocomplexes, and their interaction interfaces were characterized. Binding-free energy of specific OX40 or OX40L residue-residue interactions within 5 Å of the antibody binding interface was analyzed using Molecular Mechanics Poisson-Boltzmann Surface Area with a per-residue energy decomposition analysis. Our analysis suggests that rocatinlimab and amlitelimab directly inhibit OX40-OX40L interactions by physically blocking the cognate OX40-OX40L interface through steric occlusion, whereas telazorlimab disrupts a critical OX40-OX40L bond. Together, this work provides molecular characterization of the epitopes of OX40- and OX40L-targeted biologics emerging in dermatology. - Source: PubMed
Publication date: 2026/02/04
Nolden KelseyShi YuanjunBatista Victor SBunick Christopher G - TNFRSF4 (OX40) -TNFSF4 (OX40L) axis is the core costimulatory pathway in the TNF/TNFR superfamily that regulates T cell responses. The binding of OX40L to OX40 on the surface of activated T cells significantly enhanced the proliferation and survival of CD4 and CD8 T cells and the secretion of IFN-γ and IL-2, while inhibiting the immunosuppressive activity of regulatory T cells, thereby amplifying the anti-tumor immunity. However, although OX40 agonist monotherapy is well tolerated in phase I/II clinical trials, the objective response rate is lower than that of PD-1 monotherapy, and it does not significantly prolong progression-free survival. At the mechanistic level, insufficient affinity, limited infiltration of T cells in the tumor and residual regulatory T cells are considered to be the main bottlenecks. Despite higher objective response rates with the addition of PD-1, radiotherapy, or chemotherapy, grade 3-4 immune-related adverse events were associated with higher rates. In the future, novel OX40 agonists with high affinity and selective activation in the tumor microenvironment should be developed or incorporated into the framework of combined immunotherapy as an adjuvant strategy to achieve a balance between efficacy and safety. - Source: PubMed
Publication date: 2026/01/05
Yuan ZixuanPan YutongYuan HaodongGong Aihua