[Translation] A randomized, double-blind, placebo-controlled study to evaluate the safety, tolerability, pharmacokinetics, and pharmacodynamics of CB06-036 in patients with chronic hepatitis B

主要目的：评估在病毒抑制的慢性乙型肝炎（CHB）受试者中多次口服给药 CB06-036 后的安全性和耐受性。次要目的：评估在病毒抑制的CHB受试者中多次口服 CB06-036 后的药代动力学 (PK) 和药效学 (PD) 参数。探索性目的：（1）评价多次口服CB06-036给药后，初步的抗HBV效果；（2）评估不同基因型HBV对于CB06-036的敏感性；（3）评估 TLR8 SNP 对 CB06-036 响应的影响；

[Translation]

Primary objective: To evaluate the safety and tolerability of CB06-036 after multiple oral administration in virally suppressed chronic hepatitis B (CHB) subjects. Secondary objective: To evaluate the pharmacokinetic (PK) and pharmacodynamic (PD) parameters of CB06-036 after multiple oral administration in virally suppressed CHB subjects. Exploratory objectives: (1) To evaluate the preliminary anti-HBV effect after multiple oral administration of CB06-036; (2) To evaluate the sensitivity of different HBV genotypes to CB06-036; (3) To evaluate the effect of TLR8 SNP on the response to CB06-036;

Start Date24 Apr 2024

Sponsor / Collaborator

Shanghai Zhimeng Biopharma, Inc.Startup

NCT05828745 / RecruitingPhase 1/2

A Randomized, Double-blind, Placebo-controlled Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of Multiple Ascending Doses of CB06-036 in Subjects With Chronic Hepatitis B

CB06-036 is an investigational drug developed by Shanghai Zhimeng Biopharma Inc. for the treatment of Chronic Hepatitis B.

Start Date22 Apr 2024

Sponsor / Collaborator

Shanghai Zhimeng Biopharma, Inc.Startup

NCT06101316 / RecruitingPhase 1

A Bridging Study to Evaluate the Safety, Tolerability, and Pharmacokinetics of CB06-036 in Healthy Subjects in China

CB06-036 is an investigational drug developed by Shanghai Zhimeng Biopharma Inc. for the treatment of Chronic Hepatitis B.

Start Date19 Sep 2023

Sponsor / Collaborator

Shanghai Zhimeng Biopharma, Inc.Startup

100 Clinical Results associated with CB06

100 Translational Medicine associated with CB06

100 Patents (Medical) associated with CB06

156

Literatures (Medical) associated with CB06

01 Jun 2024·Experimental and Molecular Pathology

Effects of toll-like receptor agonists and SARS-CoV-2 antigens on interferon (IFN) expression by peripheral blood CD3+ T cells from COVID-19 patients

Article

Author: Kiaee, Fatemeh ; Garssen, Johan ; Mortaz, Esmaeil ; Bezemer, Gillina F G ; Adcock, Ian M ; Folkerts, Gert ; Sadeghi, Armin ; Abdolmohammadi-Vahid, Samaneh ; Baradaran, Behzad

BACKGROUNDSignaling by toll-like receptors (TLRs) initiates important immune responses against viral infection. The role of TLRs in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is not well elucidated. Thus, we investigated the interaction of TLRs agonists and SARS-COV-2 antigens with immune cells in vitro.MATERIAL & METHODS30 coronavirus disease 2019 (COVID-19) patients (15 severe and 15 moderate) and 10 age and sex-matched healthy control (HC) were enrolled. Peripheral blood mononuclear cells (PBMCs) were isolated and activated with TLR3, 7, 8, and 9 agonists, the spike protein (SP) of SARS-CoV-2, and the receptor binding domain (RBD) of SP. Frequencies of CD3⁺IFN-β⁺ T cells, and CD3⁺IFN-γ⁺ T cells were evaluated by flow cytometry. Interferon (IFN)-β gene expression was assessed by qRT-PCR.RESULTSThe frequency of CD3⁺IFN-β⁺ T cells was higher in PBMCs from moderate (p < 0.0001) and severe (p = 0.009) patients at baseline in comparison with HCs. The highest increase in the frequency of CD3⁺IFN-β⁺ T cells in cell from moderate patients was induced by TLR8 agonist and SP (p < 0.0001 for both) when compared to HC, while, the highest increase of the frequency of CD3⁺IFN-β⁺ T cells in sample of severe patients was seen with TLR8 and TLR7 agonists (both p = 0.002). The frequency of CD3⁺IFN-γ⁺ T cells was significantly increased upon stimulation with TLR agonists in cell from patients with moderate and severe COVID-19, compared with HC (all p < 0.01), except with TLR7 and TLR8 agonists. The TLR8 agonist did not significantly increase the frequency of CD3⁺IFN-γ⁺ T cells in PBMCs of severe patients, but did so in cells from patients with moderate disease (p = 0.01). Moreover, IFN-β gene expression was significantly upregulated in CD3⁺T cells from moderate (p < 0.0001) and severe (p = 0.002) COVID-19 patients, compared to HC after stimulation with the TLR8 agonist, while, stimulation of T cells with SP, significantly up-regulated IFN-β mRNA expression in cells from patients with moderate (p = 0.0003), but not severe disease.CONCLUSIONStimulation of PBMCs from COVID-19 patients, especially patients with moderate disease, with TLR8 agonist and SP increased the frequency of IFN-β-producing T cells and IFN-β gene expression.

23 Feb 2024·Science Immunology

UNC93B1 variants underlie TLR7-dependent autoimmunity

Article

Author: Mokhtari, Mohammad ; Siepermann, Kathrin ; Massoud, Mona ; Goetzke, Carl Christoph ; Stittrich, Anna ; Menzel, Katharina ; Kind, Barbara ; Minden, Kirsten ; Dückers, Gregor ; Engel, Kerstin ; Mages, Simon ; Bernbeck, Benedikt ; Klughammer, Johanna ; de Oliveira Mann, Carina C ; Mashreghi, Mir-Farzin ; Koss, Sarah ; Lee-Kirsch, Min Ae ; Schneider, Dominik T ; Szelinski, Franziska ; Bieringer, Markus ; Schmidt, Susanne V ; Wolf, Christine ; Durek, Pawel ; Guerra, Gabriela Maria ; Niehues, Tim ; Beltrán, Eduardo ; Majer, Olivia ; Odainic, Alexandru ; Lim, Ee Lyn ; Lara-Villacanas, Eusebia ; Dörner, Thomas ; Latz, Eicke ; Kallinich, Tilmann

UNC93B1 is critical for trafficking and function of nucleic acid–sensing Toll-like receptors (TLRs) TLR3, TLR7, TLR8, and TLR9, which are essential for antiviral immunity. Overactive TLR7 signaling induced by recognition of self–nucleic acids has been implicated in systemic lupus erythematosus (SLE). Here, we report UNC93B1 variants (E92G and R336L) in four patients with early-onset SLE. Patient cells or mouse macrophages carrying the UNC93B1 variants produced high amounts of TNF-α and IL-6 and upon stimulation with TLR7/TLR8 agonist, but not with TLR3 or TLR9 agonists. E92G causes UNC93B1 protein instability and reduced interaction with TLR7, leading to selective TLR7 hyperactivation with constitutive type I IFN signaling. Thus, UNC93B1 regulates TLR subtype–specific mechanisms of ligand recognition. Our findings establish a pivotal role for UNC93B1 in TLR7-dependent autoimmunity and highlight the therapeutic potential of targeting TLR7 in SLE.

01 Jan 2024·ChemPlusChem

Thixotropic Hydrogels Based on Laponite® and Cucurbituril for Delivery of Lipophilic Drug Molecules

Article

Author: Sainz-Díaz, C Ignacio ; Sánchez-Espejo, Rita ; Borrego-Sánchez, Ana ; Riela, Serena ; Pibiri, Ivana ; Viseras-Iborra, César ; Leone, Federica ; de Melo Barbosa, Raquel ; Cinà, Giuseppe ; Massaro, Marina ; Noto, Renato

AbstractNowadays the use of hydrogels for biomedical purposes is increasing because of their interesting features that allow the development of targeted drug delivery systems. Herein, hydrogel based on Laponite® (Lap) clay mineral as gelator and cucurbit[6]uril (CB[6]) molecules were synthetized for the delivery of flufenamic acid (FFA) for potential topical application. Firstly, the interaction between CB[6] and FFA was assessed by UV‐vis spectroscopic measurements and molecular modeling calculations. Then, the obtained complex was used as filler for Lap hydrogel (Lap/CB[6]/FFA). The properties of the hydrogel in terms of viscosity and, self‐repair abilities were investigated; its morphology was imaged by scanning electron and polarized optical microscopies. Furthermore, the changes in the hydrodynamic radii and in the colloidal stability of CB[6]/Lap mixture were investigated in terms of translational diffusion from dynamic light scattering and ζ‐potential measurements. Finally, the kinetic in vitro release of FFA, from Lap/CB[6]/FFA hydrogel, was studied in a medium mimicking the pH of skin and the obtained results were discussed both by an experimental point of view and by molecular modeling calculations.

News (Medical) associated with CB06

08 Jul 2024

·www.biospace.com

Drug Developers Tap the Immune System to Supercharge ADCs

Pictured: A white blood cell charging an ADC/Taylor Tieden for BioSpace The antibody drug conjugate market is one of the fastest growing in the pharmaceutical industry, expanding from $1 billion to $10 billion in yearly sales between 2015 to 2023—and expected to rise to $28 billion by 2028, according to Evaluate. But despite their high level of efficacy in delivering cytotoxic payloads directly to tumor cells, antibody-drug conjugates (ADCs) are “unfortunately not curing people,” Tim Lowinger, senior vice president and chief science and technology officer at Mersana Therapeutics, told BioSpace. There are real benefits, he said, including prolonged life and extended progression-free survival, yet reemergence occurs. With 15 ADCs approved as of February 2024 and many more in company pipelines, drug developers are expanding their focus to ask how they can build on the success of ADCs. Enter immunostimulatory ADCs (iADCs), sometimes called immune-stimulating antibody conjugates (iSACs). Immunotherapies are already proven cancer drugs, and delivering these treatments via ADC offers the potential to precisely target tumor cells while protecting normal cells, said Jane Chung, president and chief operating officer at Sutro Biopharma. “Engineering very targeted therapies so that you can dial up the potency of whatever payload you’re using, that’s going to . . . really move the needle on advancing cancer care,” Chung told BioSpace. Hitting the Gas on Immune Response The excitement around iADCs stems from the success of checkpoint inhibitors, said Nathan Tumey, an associate professor at Binghamton University’s School of Pharmacy and Pharmaceutical Sciences. Tumey told BioSpace that checkpoint inhibitors essentially take the brakes off of the immune system, enabling it to attack cancer cells. iADCs offer the potential to take this further and “step on the gas,” ramping up the immune response. Some of the cytotoxic payloads carried by current ADCs are also known to cause immunostimulatory cell death by creating more neoantigens in the tumor, Lowinger explained, driving companies like Pfizer to combine its auristatin-based ADC with a checkpoint inhibitor for a synergistic effect. For Lowinger, this aspect raises the question: “If a secondary mechanism of immunostimulatory cell death can have a benefit, what if you made this your primary mechanism of action?” That idea is driving interest now in iADCs. Biopharma companies are targeting a number of pathways to activate the innate immune system. Mersana, for example, is developing a stimulator of interferon genes (STING) agonist. While STING activation has known anti-cancer effects, it’s been a historically difficult target because activating it throughout the body can be toxic. The drug needs to be activated only once bound to tumor cells—which is precisely what ADCs were made to do. Using its immunosynthen platform, Mersana designed its STING agonist to stay put once delivered inside the cell with a stable, cleavable linker scaffold. Its lead asset is currently in Phase I trials against multiple HER2-positive solid tumor types. Instead of using the monoclonal antibody trastuzumab often paired with current HER2-targeting ADCs, Mersana developed a novel antibody. Therefore, it could potentially be used in combination with established, cytotoxic ADCs, as the two would not be competing for the same binding site. Meanwhile, Burlingame, CA–based Tallac Therapeutics has TAC-001, a TLR9 agonist ADC in a Phase I/II trial for solid tumors. While most ADCs carry small molecule payloads, Tallac’s platform can conjugate an oligonucleotide to an antibody, allowing modalities beyond cytotoxicity, Hong Wan, CEO of Tallac, told BioSpace. Because TLR9 is part of the innate immune system and expressed near-exclusively on immune cells, it has potential for a durable response via “immune memory,” in addition to increased safety and tolerability, Wan said. Wan pointed to the high toxicity of many current ADCs and the very high target protein expression required in the tumor to elicit the cytotoxic effect, which can restrict the efficacy to a limited patient population. In contrast, iADCs don’t require very high target expression, she said, so they could potentially benefit a broader patient population. Though data from a Phase I/II dose escalation trial have not yet been disclosed, Wan indicated the company has seen a positive response to TAC-001 in melanoma. The candidate has also been studied in the preclinical setting alongside a cancer vaccine, with positive results shared in April. And it has been combined with multiple chemotherapies preclinically. Next, Tallac is planning to test the candidate in combination with a PD1 checkpoint inhibitor. In a twist on the combination approach, South San Francisco’s Sutro—in partnership with Astellas—is taking a dual conjugation approach with its iADC. “When we put both elements, the chemotherapy and the PD1 immune activator, on an antibody . . . we reduce the tumor volume and activate the immune system to get rid of the remaining tumor cells,” said Hans-Peter Gerber, chief scientific officer at Sutro. Balancing ratios between the two elements can be precarious and the technology is critical, Gerber told BioSpace, adding that he believes Sutro stands alone in being able to dial in the correct balance. While the Astellas-partnered program does not yet have a disclosed target, Gerber said the obvious strategy would be to start in indications where immune checkpoint inhibitors already work, such as melanoma and lung and kidney cancers, then expand to populations that cannot benefit from a checkpoint inhibitor. Colorectal cancer is a “bold goal” for the company, he added. A Difficult Path The path has not been a smooth one for iADCs, though. Thanks to some highly visible clinical failures, “the field has a bad rap,” Tumey said. In 2022, an iADC combining an anti-HER2 MAB with a TLR8 agonist failed. Its developer, Silverback Therapeutics, ceased operations and became a shell company for a reverse merger with a different biotech. Two years later, Bolt Therapeutics had essentially the same results for a similar treatment. A HER2-targeting iSAC developed by Novartis also failed a Phase I trial for non-breast malignancies in 2021. “This remains a challenging area for drug discovery with considerable technical risk, as the common targets such as TLR-7, -8, -9 and STING have not yet been successfully drugged with any type of therapy,” Dan Chancellor, vice president of thought leadership at pharma solutions provider Norstella, told BioSpace in an email. He added that the iADC technology is in the beginning stages of development. However, the aforementioned three failures really amount to one, Tumey said. The companies were doing essentially the same thing—using non-cleavable linkers and effector function ADCs targeting HER2—so if one failed, “of course they’re all going to fail.” Additionally, “I think maybe a mistake that the field made early on was trying to go after breast cancer,” he said. While it seemed like the lowest hanging fruit, it’s difficult because it is an immunologically cold tumor. Like Gerber, Tumey said he believes iADCs have the highest potential in areas checkpoint inhibitors have been most successful, like non-small cell lung cancer or bladder cancer. Thanks to the success on the cytotoxic side of the ADC space, Tumey said companies appear to be more willing to take risks, potentially opening the field for meaningful success. iADCs in the Limelight In a notoriously tough biopharma funding climate, iADCs are one area drawing investment from companies. Mersana, for example, has partnerships with both GSK and Merck KGaA. The GSK deal, worth up to $1.4 billion, involves a HER2-targeted iADC currently in a Phase I dose-escalation trial. In 2022, Merck KGaA dropped $30 million up front with another $800 million on the line to conjugate Mersana’s preclinical STING-agonist to Merck KgaA’s proprietary antibodies for up to two targets. Additionally, Astellas Pharma has invested $90 million up front with Sutro to develop iADCs for three targets. Sutro could receive an additional $422.5 million in milestone payments, plus royalties. Lowinger shared the story of a study Mersana conducted treating tumors in mice with the company’s STING iADC: their tumors disappeared. Mersana then rechallenged the mice, and in mice treated with an iADC, tumors would not regrow. “This allows for the hope and dream that there’s a chance to cure patients,” Lowinger said. “I think that’s the big differentiator and why there’s interest in this approach.” Kate Goodwin is a freelance life science writer based in Des Moines, Iowa. She can be reached at kate.goodwin@biospace.com and on LinkedIn.

Phase 1VaccineImmunotherapyADC

06 Nov 2023

·www.prnewswire.com

LRA Highlights Groundbreaking Lupus Research at ACR Convergence 2023

This information is brought to you by the Lupus Research Alliance and Lupus Therapeutics and is not sponsored by, nor a part of, the American College of Rheumatology. 30+ presentations of studies funded by the LRA spanning a broad spectrum of research areas Positive results from Phase 2/3 clinical studies supported by LRA affiliate Lupus Therapeutics point to potential new treatments Lupus Therapeutics' PALS Program helps overcome challenges of diverse lupus patient trial participation SAN DIEGO, Nov. 6, 2023 /PRNewswire/ -- The Lupus Research Alliance (LRA), the largest non-governmental non-profit funder of lupus research worldwide, is pleased to announce results from more than 30 studies supported by the LRA and its clinical research affiliate Lupus Therapeutics will be presented at ACR Convergence 2023, the annual meeting of the American College of Rheumatology. Studies will represent the full continuum of research that the LRA and Lupus Therapeutics support, from innovative foundational research to lupus clinical trials evaluating potential new treatments. "The LRA and Lupus Therapeutics are extremely proud of the tremendous work we have supported that will contribute to the dynamic scientific dialogue at this important rheumatology meeting,' commented LRA President and CEO Albert T. Roy. "We also look forward to many presentations of exciting clinical research, including results from CAR-T cell therapy studies that built on pioneering work funded by the LRA and have the potential to shift the lupus treatment paradigm." FOUNDATIONAL RESEARCH FUNDED BY THE LRA LRA-funded investigators will be presenting their recent breakthroughs across a broad spectrum of lupus research, including the impact of lupus on various organs such as the skin, kidney, and brain, the contribution of the gut microbiome to lupus, dysregulation of a variety of immune cell types underlying lupus, and more. ORAL PRESENTATIONS Sunday, Nov. 12 APOL1 High Risk Genotype in SLE: A Genes in Context Story Abstract # NA, 12:00 PM – Room 11A-B ROCK1 Orchestrates B-cell Differentiation Under Stress Abstract #0729, 2:30 PM – Room 30D-E Lupus Nephritis Flares Linked to Platelet Activation During Gut Pathobiont Blooms Abstract #0851, 5:00 PM, Exhibit Hall A-B Monday, Nov. 13 CXCL13+ T cell differentiation in systemic lupus erythematosus is controlled by opposing effects of aryl hydrocarbon receptor and type I interferon Abstract #1580, 11:15 AM – Exhibit Hall A-B Metabolic Mechanisms that Control Inflammation and Immune-related Disorders Plenary Session II, 12:00 PM – Room 30D-E Keratinocyte VISTA Suppresses Skin IFN-I Production by Regulating DNA Damage Repair and Cytosolic DNA Sensing Abstract #1586, 2:15 PM – Room 32A-B Single-Cell RNA Sequencing Reveals Cellular Drivers of UV-mediated Skin Injury in Cutaneous Lupus Abstract #1599, 2:30 PM – Room 6F/6C Identifying Potential Neuroimaging Biomarkers of Neuropsychiatric Lupus in Children Using Deep Learning Abstract #1625, 3:00 PM – Room 7A-B Tuesday, Nov. 14 Longitudinal Gut Microbiome Analyses and Blooms of Pathogenic Strains during Lupus Disease Flares Abstract #NA, 8:20 AM – Room 6F/6C Development of Engineered Smith-Specific Regulatory T Cells to Treat Lupus Nephritis Abstract #2444, 2:15 PM – Room 26A-B Targeting of Endothelial Dysfunction in Lupus Nephritis: Effect on Human Renal Endothelial Cell Gene Expression and Outcomes in Murine Lupus Nephritis Abstract #2445, 2:30 PM – Room 26A-B UV Light Exposure Induces a Type I Interferon Dependent Activation and Migration of Inflammatory Dendritic Cells to Local Lymph Nodes Abstract #2448, 3:15 PM – Room 26A-B Wednesday, Nov. 15 In Situ Adaptive Immunity in Human Lupus Nephritis Abstract # N/A, 8:30 AM – Room 29A-D POSTER PRESENTATIONS – Poster Hall Sunday, Nov. 12 Elevated Serum Levels of S100A8/A9 Discriminate Systemic Lupus Erythematosus Patients with Cognitive Impairment from Patients Without Impairment Abstract #0558, 9:00 AM Comparison of Plasma Protein Profiles and Endothelial Function in Patients with Pediatric-Onset Systemic Lupus Erythematosus and Healthy Controls Abstract #0568, 9:00 AM Monday, Nov. 13 Specificity of Brain-Intrinsic and Hematopoietic-Derived Mechanisms in Mediating Neuropsychiatric Symptoms of Systemic Lupus Erythematosus Abstract #0890, 9:00 AM Adverse Childhood Experiences in a Paediatric Systemic Lupus Erythematosus Cohort Abstract #1241, 9:00 AM Agreement Between Parent- and Self-Report of Executive Function in Adolescents with Childhood-Onset Systemic Lupus Erythematosus Abstract #1242, 9:00 AM Proinflammatory Neutrophils and NETs Mediate Skin and Kidney Inflammation During Lupus Flare in Asymptomatic Lupus-prone Mice Triggered by UVB Abstract #0920, 9:00 AM IL-4 Acts Through Aryl Hydrocarbon Receptor to Antagonize TLR7-induced Double Negative 2 B Cells in Lupus Abstract #0925, 9:00 AM Examining the Relationship Between Socioenvironmental Factors and Cognitive Functioning in Youth with Childhood-Onset Systemic Lupus Erythematosus Abstract #1226, 9:00 AM Longitudinal Assessment of Self-reported Executive Function in Youth with Childhood-Onset Lupus Abstract #1229, 9:00 AM Complement Deposition on Extracellular Mitochondria Induces Platelet Activation in Vitro Abstract #0900, 9:00 AM The Cellular and Spatial Type I Interferon Response Following Skin Exposure to Ultraviolet Light Abstract #0894, 9:00 AM Tuesday, Nov. 14 Brain Activity Patterns and Behavioural Performance in SLE Patients During a Spatial Working Memory and Sustained Attention Task Abstract #2258, 9:00 AM The Effects of Systematic Lupus Erythematosus Related Cognitive Impairments on Activities of Daily Living and Life Role Participation: A Qualitative Framework Study Abstract #2259, 9:00 AM Association of Mycophenolate and Azathioprine Use with Cognitive Function in Systemic Lupus Using a Bayesian Longitudinal Item-response Theory Model Abstract #2290, 9:00 AM CLINICAL TRIALS SUPPORTED BY LUPUS THERAPEUTICS As the clinical research affiliate of the LRA, Lupus Therapeutics collaborates with biotechnology and pharmaceutical companies, as well as lupus experts from their Lupus Clinical Investigators Network (LuCIN) to help design and conduct high-quality, patient-centric, and diverse lupus studies, including several with results being presented at ACR Convergence 2023. ORAL PRESENTATIONS Tuesday, Nov. 14 Efficacy and Safety of ABBV-599 High Dose (Elsubrutinib 60 mg and Upadacitinib 30 mg) and Upadacitinib Monotherapy for the Treatment of Systemic Lupus Erythematosus: A Phase 2, Double-blind, Placebo-controlled Trial Abstract #2488, 2:00 PM – Ballroom 20D Phase 2 Safety and Efficacy of Subcutaneous (s.c.) Dose Ianalumab (VAY736; Anti-BAFFR mAb) Administered Monthly over 28 Weeks in Patients Abstract #2487, 2:00 PM – Ballroom 20D POSTER PRESENTATIONS – Poster Hall Monday, Nov. 13 Treatment with Upadacitinib in Patients with Systemic Lupus Erythematosus Results in the Inhibition of B-Cell–related Biomarkers: Analysis of the M19-130 (SLEek) Phase 2 Study Abstract #1489, 9:00 AM Disease Course and Complement as Predictors of Response to Standard of Care Plus Placebo in Patients with SLE: A Post Hoc Analysis of Dapirolizumab Pegol and Epratuzumab Clinical Trial Data Abstract #1503, 9:00 AM Steroid-sparing Effects of Afimetoran (BMS-986256), an Equipotent Toll-like Receptor (TLR)7 and TLR8 Antagonist, in a Lupus Mouse Model Abstract #0897, 9:00 AM Transcriptomic Analysis of the Impact of Iberdomide on Patients with SLE Abstract #1694, 4:00 PM Tuesday, Nov. 14 Dapirolizumab Pegol Impacts Important Immunologic Pathways in SLE: Pharmacodynamic Analysis of B Cell and Type I Interferon Pathways from a Phase 2b Trial Abstract #2333, 9:00 AM Modulation of B Cell and Interferon Pathways by Ianalumab in Patients with Systemic Lupus Erythematosus: Findings from a Phase 2 Clinical Trial Abstract #2342, 9:00 AM WORK CONDUCTED THROUGH THE LUPUS THERAPEUTICS PALS PROGRAM Patient Advocates for Lupus Studies (PALS) is a peer support program that aims to improve participation in lupus clinical trials through increased education and availability of information about clinical trials. Individuals living with lupus who have clinical research act as peer educators, or PALs, to deliver educational sessions to others living with lupus. The PALS program was piloted from 2019-2021 and demonstrated significant increases in knowledge about, attitudes toward, and intentions to participate in lupus clinical trials among program participants. POSTER PRESENTATION – Poster Hall Sunday, Nov. 12 Barriers and Facilitators to Recruiting Underrepresented Participants for Clinical Trials: Insights from the Lupus Clinical Investigators Network (LuCIN) Abstract #0183, 9:00 AM WORK CONDUCTED BY THE ACCELERATING MEDICINES PARTNERSHIP The LRA is a partner in Accelerating Medicines Partnership® Autoimmune Mediated Disease (AMP® AIM), which brings together 20 organizations from the public, private, and nonprofit sectors to accelerate the identification and validation of new therapeutic targets by reconstructing shared immune response pathways through spatial and multi-omics technologies. The project is managed by the FNIH and builds on the success of AMP RA/SLE in which LRA was also a partner. The presentation of results from an AMP® AIM lupus study is noted below. ORAL PRESENTATION Monday, Nov. 13 Single Cell Transcriptomics in Kidney Tissue from African American Patients Enrolled in the Accelerating Medicines Partnership (AMP) Implicates Tubular Cells in the Pathogenesis of APOL1 Associated Lupus Nephritis Abstract #1695, 4:30 PM – Room 6F/6C About Lupus Lupus is a chronic, complex autoimmune disease that affects millions of people worldwide. More than 90 percent of people with lupus are women, often striking during the childbearing years of 15-45. Blacks/African Americans, Hispanics, Asians, and Native Americans are at two to three times greater risk than Caucasians for developing lupus. In lupus, the immune system, meant to defend against infections, produces antibodies that mistakenly recognize the body's own cells as foreign, prompting other immune cells to attack and potentially damage organs such as the kidneys, brain, heart, lungs, blood, skin, and joints. About Lupus Research Alliance The Lupus Research Alliance is the largest non-governmental, non-profit funder of lupus research worldwide. The organization aims to transform treatment by funding the most innovative lupus research, fostering diverse scientific talent, and driving discovery toward better diagnostics, improved treatments and ultimately, cure for lupus. Because the Lupus Research Alliance's Board of Directors funds all administrative and fundraising costs, 100% of all donations goes to support lupus research programs. About Lupus Therapeutics Lupus Therapeutics, the clinical research affiliate of the Lupus Research Alliance, aims to accelerate the development of curative treatments for all patients living with lupus. Lupus Therapeutics collaborates with academic institutions, biotechnology, and pharmaceutical partners through the unprecedented Lupus Clinical Investigators Network (LuCIN) to drive rapid and meaningful progress in the treatment of lupus patients. The organization elevates the patient voice, engages community stakeholders, and strives for representation of the diverse lupus community in the clinical research process with the most innovative and renowned experts throughout North America. Visit lupustherapeutics.org for more information. SOURCE Lupus Research Alliance

Phase 2Clinical Result

01 Feb 2023

·www.core-biopharma.com

Zhimeng Biopharma Entered into A Global Exclusive Licensing Agreement with GlaxoSmithKline in HBV

In December 2022, Zhimeng Biopharma entered into a Global Exclusive license agreement with GSK for CB06, a TLR8 agonist. Subject to successful completion of phase I, the agreement will allow GSK to develop, manufacture and commercialise CB06 for the treatment of HBV. If successful, CB06 could be used in combination, or as a sequential treatment with bepirovirsen, to potentially deliver a functional cure in more HBV patients.

License out/inPhase 1

100 Deals associated with CB06

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Indication	Highest Phase	Country/Location	Organization	Date
Hepatitis B, Chronic	Phase 2	CN	Shanghai Zhimeng Biopharma, Inc.Startup	22 Apr 2024

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