A Phase 2b/3, Multi-part, Randomized, Double-Blinded, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Atacicept in Subjects with IgA Nephropathy (IgAN)

开始日期2023-11-15

申办/合作机构

Vera Therapeutics, Inc.

NCT04716231 / Recruiting临床3期

A Phase 2b/3, Multi-part, Randomized, Double-Blinded, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Atacicept in Subjects with IgA Nephropathy (IgAN)

A Phase 3 Study with Atacicept in Subjects With IgA Nephropathy (ORIGIN 3)

开始日期2023-05-23

申办/合作机构

Vera Therapeutics, Inc.

NCT05609812 / Suspended临床3期

A Phase 3 Randomized, Double-Blind, Placebo-Controlled Multicenter, Multinational Study to Evaluate the Efficacy and Safety of Atacicept in Subjects With Active Lupus Nephritis

The objective of the study is to evaluate the effect of atacicept compared to placebo on changes to renal response in adult subjects with LN.

开始日期2022-11-02

申办/合作机构

Vera Therapeutics, Inc.

100 项与 Vera Therapeutics, Inc. 相关的临床结果

登录后查看更多信息

0 项与 Vera Therapeutics, Inc. 相关的专利（医药）

登录后查看更多信息

项与 Vera Therapeutics, Inc. 相关的文献（医药）

2024-06-01·Kidney International

A phase 2b, randomized, double-blind, placebo-controlled, clinical trial of atacicept for treatment of IgA nephropathy

Article

作者: Jha, Vivekanand ; Lafayette, Richard ; Tesař, Vladimír ; Barratt, Jonathan ; Maes, Bart ; Kim, Sung Gyun ; Israni, Rubeen ; Floege, Jürgen ; Singh, Harmeet ; Eren, Necmi ; Wei, Xuelian ; Barbour, Sean ; Lin, Celia J F ; Phoon, Richard K S

Atacicept is a first-in-class, dual anti-B-cell Activation Factor-A Proliferation-Inducing Ligand fusion protein in clinical evaluation for treatment of IgA nephropathy. To compare efficacy and safety of atacicept versus placebo in patients with IgAN, this randomized, double-blind, placebo-controlled phase 2b clinical trial ORIGIN enrolled 116 individuals with biopsy-proven IgA nephropathy. Participants were randomized to atacicept 150, 75, or 25 mg versus placebo once weekly for up to 36 weeks. Primary and key secondary endpoints were changes in urine protein creatinine ratio based on 24-hour urine collection at weeks 24 and 36, respectively, in the combined atacicept 150 mg and 75 mg group versus placebo. The primary endpoint was met at week 24 as the mean urine protein creatinine ratio was reduced from baseline by 31% in the combined atacicept group versus 8% with placebo, resulting in a significant 25% reduction with atacicept versus placebo. At week 36, the key secondary endpoint was met as the mean urine protein creatinine ratio reduced from baseline by 34% in the combined atacicept group versus a 2% increase with placebo, resulting in a significant 35% reduction with atacicept versus placebo. The reduction in proteinuria was accompanied by stabilization in endpoint eGFR with atacicept compared to a decline with placebo at week 36, resulting in significant between-group geometric mean difference of 11%, approximating an absolute difference of 5.7 mL/min/1.73m². Endpoint galactose deficient IgA1 levels significantly decreased from baseline by 60% versus placebo. The safety profile of atacicept was like placebo. Thus, our results provide evidence to support a pivotal, phase 3 study of atacicept in IgA nephropathy.

2024-05-23·Nephrology Dialysis Transplantation

#812 Phase 2b ORIGIN study open label extension with atacicept in patients with IgA nephropathy and persistent proteinuria: week 72 interim analysis

作者: Phoon, Richard ; Israni, Rubeen ; Floege, Jürgen ; Jha, Vivekanand ; Barratt, Jonathan ; Lin, Celia ; Tesar, Vladimir ; Barbour, Sean ; Maes, Bart ; Lafayette, Richard ; Wei, Xuelian ; Kim, Sung Gyun

AbstractBackground and AimsIgA nephropathy (IgAN), the most common primary glomerulonephritis and a significant contributor to ESKD worldwide, is characterized by elevated serum levels of galactose-deficient IgA1 (Gd-IgA1). The production of Gd-IgA1 and its autoantibodies is driven by both the B-cell Activating Factor (BAFF) and A PRoliferation-Inducing Ligand (APRIL) signaling pathways that stimulate maturation, differentiation, and effector function of B cells and plasma cells. Atacicept is a fusion protein targeting both BAFF and APRIL in clinical development for IgAN treatment. The Phase 2b ORIGIN study met the primary endpoint with statistically significant urine protein:creatinine ratio (UPCR) reduction at 24 weeks vs placebo. At 36 weeks, atacicept 150 mg achieved statistically significant and clinically meaningful UPCR reduction, eGFR stabilization, and Gd-IgA1 reduction vs placebo, with similar safety to placebo. This interim analysis reports 72-week results from the open-label extension period.MethodThe randomized, double-blind, placebo-controlled Phase 2b ORIGIN study included 116 participants with biopsy-proven IgAN, 24 h urine protein >0.75 g/day or UPCR >0.75 g/g, and eGFR ≥30 mL/min/1.73 m2 despite optimized renin–angiotensin system blockade. Participants were randomized to atacicept 150, 75, or 25 mg, vs placebo (2:2:1:2), self-administered by subcutaneous injection once weekly for up to 36 weeks. The double-blind randomized treatment period was followed by an open-label extension in which participants could receive atacicept 150 mg for up to 60 additional weeks, for a total of 96 weeks. For this interim analysis, changes from baseline in eGFR, natural log transformed UPCR, and Gd-IgA1 through 72 weeks were analyzed using a mixed-effects model for repeated measurements. Microscopic hematuria was evaluated on urine dipstick and participants with hematuria grade 1+ or higher at baseline were evaluated for resolution, defined as a decrease to negative/trace, at 72 weeks.ResultsOf 116 randomized participants in the double-blind period, 106 participants (91%) completed 72 weeks of treatment. At 72 weeks, eGFR total slope estimate was 0.0 mL/min/1.73m2/year and eGFR change from baseline was 0 mL/min/1.73m2 in all participants originally randomized to atacicept (all-atacicept group; n = 82). After switching to open-label atacicept 150 mg, the original placebo group showed eGFR stabilization with −3.2 mL/min/1.73m2 change from baseline at 72 weeks vs −4.9 mL/min/1.73m2 at 36 weeks (Figure 1). At 72 weeks, UPCR change from baseline was −45% in the all-atacicept group and the placebo switch group showed a −47% UPCR change from baseline at 72 weeks vs +3% at 36 weeks (Figure 2). Open-label atacicept 150 mg was also associated with rapid Gd-IgA1 reduction in the placebo switch group at 48 weeks that was sustained through 72 weeks. Hematuria resolution was observed at 72 weeks in 81% (35/43) of participants in the all-atacicept group and 59% (10/17) in the placebo switch group. Atacicept was generally well tolerated during the open-label extension, with a similar rate of infections compared to the double-blind period and one study drug-related serious adverse event.ConclusionAt 72 weeks, treatment with atacicept 150 mg was associated with sustained eGFR stability and deepening UPCR reductions, as well as a reversal of the downward eGFR decline in the placebo switch group. Sustained reductions in hematuria were also observed. The open-label extension showed a favorable safety profile similar to the double-blind period. These results support atacicept 150 mg as a potential disease-modifying treatment for IgAN.

2024-05-23·Nephrology Dialysis Transplantation

#123 Impact of atacicept on hematuria in IGA nephropathy: post-hoc analysis of the phase 2b ORIGIN study

作者: Phoon, Richard ; Kim, Sung Gyun ; Wei, Xuelian ; Lafayette, Richard ; Jha, Vivekanand ; Wadhwani, Shikha ; Barratt, Jonathan ; Floege, Jürgen ; Cooper, Kerry ; Barbour, Sean ; Maes, Bart ; Lin, Celia ; Tesar, Vladimir

AbstractBackground and AimsPatients with IgA nephropathy (IgAN) and persistent hematuria during follow up have a greater decline in renal function than those with minimal or no hematuria, while hematuria resolution has been independently associated with less decline in renal function [1, 2]. Atacicept is a fusion protein targeting both BAFF and APRIL in clinical development for IgAN. The Phase 2b ORIGIN study met the primary endpoint with statistically significant urine protein:creatinine ratio (UPCR) reduction at 24 weeks for atacicept vs placebo. At 36 weeks, atacicept 150 mg achieved statistically significant and clinically meaningful UPCR reduction, eGFR stabilization, and robust reduction of galactose-deficient IgA1 vs placebo, with similar safety to placebo. This post-hoc analysis evaluates changes in hematuria during treatment with atacicept vs placebo over 36 weeks.MethodThe randomized, double-blind, placebo-controlled Phase 2b ORIGIN study included 116 participants with biopsy-proven IgAN, 24h urine protein >0.75 g/day or UPCR >0.75 g/g, and eGFR ≥30 mL/min/1.73 m2 despite optimized renin–angiotensin system blockade. Participants were randomized to atacicept 150, 75, or 25 mg vs placebo (2:2:1:2) self-administered by subcutaneous injection once weekly for up to 36 weeks. Microscopic hematuria was evaluated at weeks 2, 4, 12, 24, and 36 via urine dipstick at a centralized lab, and hematuria levels were graded negative/trace, 1+, 2+, or 3+. Hematuria improvement was defined as a decrease by ≥1 grade, and resolution was defined as a decrease to negative/trace.ResultsIn the intent-to-treat population, 15 of 33 (45%) participants who received atacicept 150 mg and 19 of 34 (56%) who received placebo had hematuria (1+ or greater) at baseline. Of these, 87% (n = 13/15) on atacicept 150 mg had improved hematuria at 36 weeks vs 32% (n = 6/19) on placebo (p = 0.002), with 80% (n = 12/15) on atacicept 150 mg achieving resolution to negative/trace hematuria vs 5% (n = 1/19) on placebo (p < 0.0001) (Figure). The atacicept 150 mg group steadily improved to lower hematuria grades over 36 weeks, with improvement occurring as early as 4 weeks, while the placebo group had no improvement in hematuria over time. The majority of participants without hematuria at baseline maintained negative or trace levels at 36 weeks.ConclusionIn a post-hoc analysis, atacicept treatment was associated with hematuria resolution at 36 weeks in a substantially greater percentage of participants as compared with placebo, with improvements seen as early as 4 weeks. These results add to the growing body of evidence supporting atacicept as a potential disease-modifying treatment for IgAN. Atacicept 150 mg is currently being evaluated in a global Phase 3 randomized placebo-controlled trial.

101

项与 Vera Therapeutics, Inc. 相关的新闻（医药）

2024-10-30

·GlobeNewswire-Health Care

Vera Therapeutics Announces Pricing of Public Offering of Class A Common Stock

BRISBANE, Calif., Oct. 29, 2024 (GLOBE NEWSWIRE) -- Vera Therapeutics, Inc. (“Vera”), a late clinical-stage biotechnology company focused on developing and commercializing transformative treatments for patients with serious immunologic diseases, today announced the pricing of an underwritten public offering of 7,142,858 shares of its Class A common stock at a price to the public of $42.00 per share. The gross proceeds to Vera from the offering, before deducting underwriting discounts and commissions and estimated offering expenses, are expected to be approximately $300.0 million. In addition, Vera has granted the underwriters a 30-day option to purchase up to an additional 1,071,428 shares of Class A common stock at the public offering price, less underwriting discounts and commissions. The offering is expected to close on October 31, 2024, subject to the satisfaction of customary closing conditions. J.P. Morgan, Goldman Sachs & Co. LLC, Evercore ISI and Cantor are acting as joint book-running managers for the proposed offering. The proposed offering is being made pursuant to an automatic shelf registration statement on Form S-3, including a base prospectus, that was filed with the Securities and Exchange Commission (the “SEC”) on October 28, 2024 and became effective upon filing. A preliminary prospectus supplement and accompanying prospectus relating to the proposed offering were filed with the SEC and are available for free on the SEC’s website located at http://www.sec.gov. A final prospectus supplement and accompanying prospectus relating to the proposed offering will be filed with the SEC and will be available for free on the SEC’s website located at http://www.sec.gov. Copies of the final prospectus supplement and the accompanying prospectus relating to the offering may be obtained, when available from: J.P. Morgan Securities LLC, c/o Broadridge Financial Solutions, 1155 Long Island Avenue, Edgewood, NY 11717, by email at prospectus-eq_fi@jpmchase.com and postsalemanualrequests@broadridge.com; Goldman Sachs & Co. LLC, Attention: Prospectus Department, 200 West Street, New York, NY 10282, or by telephone at (866) 471-2526, or by email at prospectus-ny@ny.email.gs.com; Evercore Group L.L.C., Attention: Equity Capital Markets, 55 East 52nd Street, 35th Floor, New York, NY 10055, or by telephone at 888-474-0200, or by email at ecm.prospectus@evercore.com; or Cantor Fitzgerald & Co., Attention: Capital Markets, 110 East 59th St., 6th Floor, New York, NY 10022, or by email at prospectus@cantor.com. This press release shall not constitute an offer to sell or a solicitation of an offer to buy, nor shall there be any sale of these securities in any state or jurisdiction in which such offer, solicitation or sale would be unlawful prior to registration or qualification under the securities laws of any such state or jurisdiction. About Vera Vera is a late clinical-stage biotechnology company focused on developing treatments for serious immunological diseases. Vera’s mission is to advance treatments that target the source of immunological diseases in order to change the standard of care for patients. Vera’s lead product candidate is atacicept, a fusion protein self-administered as a subcutaneous injection once weekly that blocks both B-cell activating factor (BAFF) and A proliferation-inducing ligand (APRIL), which stimulate B cells and plasma cells to produce autoantibodies contributing to certain autoimmune diseases, including IgAN, also known as Berger’s disease, and lupus nephritis. In addition, Vera is evaluating additional diseases where the reduction of autoantibodies by atacicept may prove medically useful. Vera is also developing MAU868, a monoclonal antibody designed to neutralize infection with BK virus (BKV), a polyomavirus that can have devastating consequences in certain settings such as kidney transplant. Vera retains all global developmental and commercial rights to atacicept and MAU868. Forward-looking Statements Statements contained in this press release regarding Vera’s expectations regarding the offering are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. These forward-looking statements are based upon Vera’s current expectations and involve assumptions that may never materialize or may prove to be incorrect. Actual results could differ materially from those anticipated in such forward-looking statements as a result of various risks and uncertainties, which include, without limitation, Vera’s expectations regarding the completion of the offering. All forward-looking statements contained in this press release speak only as of the date on which they were made and are based on management’s assumptions and estimates as of such date. Vera undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made, except as required by law. Investor Contact: Joyce AllaireLifeSci Advisors212-915-2569jallaire@lifesciadvisors.com Media Contact: Madelin HawtinLifeSci CommunicationsMHawtin@lifescicomms.com

临床研究免疫疗法

2024-10-29

·EndPoints

Vera’s $300M offering; Abeona resubmits treatment for rare skin disease

Plus, news about Astellas, Clover, ElevateBio, Monopar, Idorsia and Neurocrine Biosciences: Vera Therapeutics plans $300M offering: The California biotech is selling shares after presenting Phase 2b data for an experimental drug called atacicept over the weekend. The company shared 96-week data for patients with immunoglobulin A nephropathy. — Kyle LaHucik Abeona Therapeutics resubmits rare skin disease therapy: Back in April, the FDA rejected Abeona’s cell therapy, called pz-cel, requesting more information about manufacturing. Abeona is developing pz-cel for recessive dystrophic epidermolysis bullosa, a rare genetic skin disease. — Lei Lei Wu Astellas yanks Izervay’s submission in Europe: The company said it withdrew its marketing authorization application for Izervay, a C5 protein inhibitor for geographic atrophy secondary to age-related macular degeneration. Astellas did not detail feedback from the Committee for Medicinal Products for Human Use, but said it is still “confident” in Izervay’s risk-benefit profile and will continue to engage with regulators in Europe and elsewhere. There are currently no treatments approved for GA secondary to AMD outside of the US, where Izervay was greenlit in August of last year. — Ayisha Sharma Clover releases early RSV vaccine data: The Shanghai-based biotech said its bivalent vaccine candidate, SCB-1019, produced “comparable” levels of RSV neutralizing antibodies to GSK’s Arexvy at 28 days in a Phase 1 test. Based on these data, Clover plans to advance the asset into studies focused on re-vaccination next year. — Ayisha Sharma ElevateBio lays off 4%: The genetic medicines company, which employs about 500 people, is ending its preclinical cellular engineering work, a spokesperson told Endpoints News on Monday. The Waltham, MA-based biotech laid off about 13% of its staff in October 2023. It’s one of the most well-funded private biopharma startups after having raised about $1.25 billion, including its $401 million Series D last year. Partnerships with companies like Novo Nordisk, Moderna, Kyverna and Affini-T are unaffected, the spokesperson confirmed. — Kyle LaHucik Monopar Therapeutics prices $19.2M offering: The Chicago-area biotech sold shares to Janus Henderson, RA Capital and others. A few days ago, Monopar licensed a Wilson disease drug candidate from AstraZeneca’s Alexion. — Kyle LaHucik Idorsia ends work with Neurocrine Biosciences: The companies were developing Idorsia’s T-type calcium channel blocker for patients with a rare form of pediatric epilepsy. The treatment failed a Phase 2 study in 2022, and further analysis led to the decision to stop work. — Jaimy Lee

疫苗临床2期上市批准

2024-10-28

·药研网

BAFF-APRIL系统：自免、肿瘤领域潜力无限

BAFF（B细胞激活因子,也称为TNFSF13B、CD257、BLys）和APRIL（增殖诱导配体，也称为CD256，TNFSF13）参与了许多人类自身免疫性疾病的发生，在系统性红斑狼疮(SLE)、IgA肾病、Sjögren’s综合征和类风湿关节炎患者的血清中检测到这些细胞因子水平升高。因此，这两种分子都是B细胞驱动的自身免疫性疾病的合理治疗靶点，一些BAFF/APRIL的抑制剂已经在临床试验中取得成功并获批上市。其中包括BAFF抑制剂贝利尤单抗和BAFF/APRIL双靶抑制剂泰它西普。 BAFF/APRIL系统概述 BAFF和APRIL都属于B细胞刺激因子，是维持B细胞和体液免疫的关键因素。 BAFF属于肿瘤坏死因子（TNF）配体家族成员，表达于单核细胞、树突状细胞及T细胞等表面。BAFF也可以从细胞表面分离，进入血液中形成可溶性分子。 BAFF 主要通过与B细胞表面的三种受体结合发挥作用，分别是：BAFFR(BAFF受体，也被称为BR3和TNF受体超家族成员13C)，TACI(钙调和亲环素配基相互作用因子，也称为TNF受体超家族成员13B)，BCMA(B细胞成熟抗原，也称为TNF受体超家族成员17)。 BAFF通过与其受体的结合在支持B细胞的存活和增殖、调节类别转换重组以及自身免疫性B细胞的选择等方面发挥关键作用；此外，有研究发现BAFF也能促进T细胞的活化、增殖和分化。 APRIL 和BAFF具有结构相似性，都是属于肿瘤坏死因子（TNF）超家族的成员。与BAFF不同，APRIL仅与TACI和BCMA（而非BAFF-R）结合以调节B细胞的功能和存活，并促进其分化为浆细胞。在健康人组织中，APRIL的表达相对较弱，而在肿瘤组织中却高表达。APRIL有两种生物活性存在形式，分别是以17k相对分子质量存在的可溶型和30k相对分子质量存在的膜结合型。研究显示，BAFF相对于APRIL对BAFF-R的结合有更强的特异性，但BCMA对APRIL的亲和力更高。图1.BAFF与BAFFR的配体受体结合图（DOI：10.1038/ng0805-793） BAFF-APRIL系统的临床价值 01 BAFF/BAFFR BAFF及其受体BAFFR在B细胞的生理和病理过程中发挥关键作用，针对这两个分子的靶向治疗已经成为自身免疫性疾病和相关恶性疾病的一种有效策略。 BAFF与BAFFR的结合能激活多个信号通路，包括NF-κB和PI3K，这些信号通路在B细胞存活和增殖中发挥重要作用。 BAFF和BAFFR的相互作用在临床上被用作治疗靶点。例如，贝利尤单抗（Benlysta）是针对BAFF的单克隆抗体，已被批准用于治疗系统性红斑狼疮等疾病。此外，针对BAFFR的靶向药物也在开发中，显示出治疗慢性淋巴细胞白血病和其他B细胞相关淋巴瘤潜力。迄今为止，全球尚未有针对BAFF-R的靶向药物获监管机构批准应用于临床治疗。图2.BAFF-BAFFR靶点全球在研项目汇总吉满生物自主研发，推出一系列BAFF和APRIL系统相关靶点的稳定过表达细胞系、报告基因检测细胞系、抗体及蛋白相关产品，充分满足药物研发需求，助力药物临床申报。详情咨询吉满客服联系同微信：18916119826！ Ianalumab Ianalumab是一种抗BAFF-R的单克隆抗体，在治疗干燥综合征和系统性红斑狼疮的2期临床试验中均获得积极结果，目前正在3期临床试验中接受检验。 PMB-101 PMB-CT01是一种潜在“first-in-class”的BAFFR靶向自体CAR-T细胞疗法。临床前研究发现，这种CAR-T细胞疗法能在体外和动物模型中杀死人类淋巴瘤和白血病细胞。2024年1月19日，PeproMene Bio宣布，其PMB-CT01在治疗复发/难治性急性B淋巴细胞白血病（r/r B-ALL）的1期临床试验中获得积极结果。第1队列首例患者在治疗后一个月得到完全缓解。 AUR200 AUR200 是一种高效、特异性的 BAFF 和 APRIL 活性免疫调节剂，AUR200 的作用机制已得到证实。Aurinia于2024年第三季度启动了AUR200的1期单剂量（SAD）研究。SAD研究的数据，包括安全性、耐受性、药代动力学和生物标志物，预计将于2025年上半年公布。 ESG206 诗健生物同类首创抗BAFF-R单克隆抗体ESG206，可通过抗体依赖的细胞介导的细胞毒性作用（ADCC）发挥肿瘤细胞杀伤效能。通过糖基化修饰使得ESG206无岩藻糖基化糖型的含量大大提高从而显著增强体外的ADCC作用。 ESG206拟应用于B细胞淋巴瘤和慢性淋巴细胞白血病，特别是对现有治疗耐药的B淋巴细胞瘤。目前该管线在中国和澳大利亚的临床申请均已获批。此外，ESG206后续还将开展自身免疫疾病治疗的开发和探索。安博泰克JH013注射液 8 月 2 日，安博泰克公司治疗自身免疫性疾病的抗BAFF-R单克隆抗体JH013注射液获得国家药品监督管理局颁发的临床研究（IND），这是首个获得临床研究批件的国产BAFF-R单克隆抗体。临床前研究证实，JH013 可以从蛋白水平及细胞水平与人BAFF-R呈线性结合，并且阻断 BAFF-R 与 BAFF 的相互作用，从而抑制 BAFF 引起的 B 淋巴细胞增殖。 023 TACI TACI作为BAFF的受体，其作用不局限于B细胞的生存和功能调节，还在T细胞的活化和成熟中发挥重要的交互调控作用。 BAFF与TACI之间的相互作用在多种自身免疫疾病（例如系统性红斑狼疮、类风湿性关节炎等）中被认为是病理机制的重要组成部分。近几年来，TACI靶点迅速变得火热，围绕该靶点，研发进展靠前的药物有Vera的Atacicept，荣昌生物的Telitacicept，Alpine的Povetacicept 等。 Vera：Atacicept Atacicept是可溶性全人源化的 TACIFc 融合蛋白，可与 BAFF 和 APRIL 这 2 种配体结合。Vera Therapeutics引进之后，Atacicept的临床开发重新走上正轨，目前IgA肾病三期临床正在进行，狼疮性肾炎、系统性红斑狼疮计划推进到三期临床，后续还有多个适应症处在早期临床阶段。荣昌生物：Telitacicept 泰它西普（Telitacicept，商品名：泰爱）是荣昌生物自主研发的靶向 BLyS 和 APRIL 的原创性抗体融合蛋白药物，用于治疗系统性红斑狼疮、类风湿性关节炎等多种自身免疫疾病。 2021年3月，泰它西普在中国附条件获批上市，治疗系统性红斑狼疮，成为全球首款TACI-Fc新药。 Alpine：Povetacicept Povetacicept目前进展最快的为IgA肾病，今年下半年将启动三期关键临床，后续探索的适应症还有系统性红斑狼疮、膜性肾病、血球减少症。 03 BCMA BCMA可分别与BAFF或APRIL两种配体相结合。其主要功能是调节B细胞的生存和成熟。在多发性骨髓瘤细胞中，BCMA的过度表达与疾病的恶性转化过程密切相关，是用于治疗多发性骨髓瘤（MM）的一个重要靶点。近年来，针对BCMA的不同类型免疫治疗药物得到了广泛的开发，主要分为三类：嵌合抗原受体T细胞（CAR-T）疗法、双特异性抗体（BsAb）和抗体药物偶联物（ADC）。（1）CAR-T细胞疗法 CAR-T细胞疗法是目前针对BCMA的最活跃的研发领域之一。此类疗法通过对患者T细胞进行基因工程修饰，使其表达对BCMA特异的CAR，能够识别并攻击表达BCMA的肿瘤细胞。目前已有多个BCMA靶向CAR-T细胞疗法获得审批，如百时美施贵宝的Abecma和强生的Cilta-cel，这些疗法在复发或难治性多发性骨髓瘤患者中显示出显著疗效。（2）双特异性抗体（BsAb）双特异性抗体通过同时结合BCMA和T细胞表面抗原，使这两种细胞相互靠近，增强T细胞对肿瘤细胞的杀伤能力。此类药物的代表有Teclistamab，它是第一个获得FDA批准的靶向BCMA的双特异性抗体，也是是全球首个BCMA/CD3双特异性抗体，针对复发或难治性多发性骨髓瘤患者。（3）抗体药物偶联物（ADC）抗体药物偶联物则是将抗体与细胞毒性药物结合，通过靶向BCMA直接将药物传递至恶性浆细胞。这类药物例如Belantamab mafodotin（Blenrep），在FDA批准后显著改善了多发性骨髓瘤的治疗效果。 04 APRIL APRIL主要在B细胞和浆细胞中表达，可以结合TACI和BCMA，从而影响B细胞的增殖和分化。特别是APRIL在自身免疫性疾病中，通过促进自身抗体的产生，起到了重要的病理角色。 APRIL的靶点药物开发近年来受到了广泛关注，特别是在自身免疫性疾病和某些肿瘤治疗领域。目前进展最快的是大冢制药的Sebeprenlimab（VIS649），它是一款抗APRIL单抗。10月22日，大冢制药宣布Sebeprenlimab治疗IgA肾病的三期临床VISIONARY达到预设主要终点，经过9个月治疗24小时uPCR（尿蛋白肌酐比）显著下降，安全性与此前报道的数据一致。总结总的来说，BAFF和APRIL系统相关的靶向药物，未来临床应用前景广阔，尤其是在自身免疫疾病和肿瘤免疫治疗领域。正在进行的临床研究将进一步验证这些生物制剂的长期疗效和安全性，尤其是在不同患者群体中的应用效果。我们期待能为治疗相关疾病提供新的策略。用心做好细胞，为更好的靶向药吉满生物自主研发，推出一系列BAFF和APRIL系统相关靶点的稳定过表达细胞系、报告基因检测细胞系、抗体及蛋白相关产品，充分满足药物研发需求，助力药物临床申报。吉满优势高稳定性：我们的稳转细胞株经过严格筛选，确保在长期培养中保持高稳定性，适合大规模生产和长期实验使用纯度和活性：我们的蛋白、抗体产品经过高效纯化，确保高纯度和生物活性，适合用于基础研究、药物开发和临床前研究定制服务：我们提供个性化的定制服务，根据客户的具体需求，开发特定的细胞株、抗体和蛋白，满足不同研究领域的需求技术支持：我们的专业团队提供全面的技术支持和咨询服务，帮助客户解决在使用产品过程中遇到的各种问题可靠性和信誉：我们在行业内拥有良好的声誉，客户反馈积极，产品质量和服务得到了广泛认可产品列表数据展示（部分） GM-C25349:H_BCMA Reporter Cell Line 使用Recombinant Human APRIL(N-Flag-His)(novoprotein/CU89)蛋白激活验证使用Recombinant Human APRIL (N-Flag-His) (novoprotein/CU89)蛋白激活后，在分别使用Anti-BCMA hIgG1 Antibody(SEA-BCMA)、Anti-BCMA hIgG1 Antibody(Belantamab) 抗体block验证 GM-C31635:H_BAFFR Reporter Cell Line 使用Human BAFF Protein; His Tag蛋白激活验证使用Human BAFF Protein激活后，在使用Anti-BAFF hlgG1 Antibody(belimumab)抗体block验证结果 GM-C35041:H_TACI Reporter Cell Line 使用Human BAFF Protein; His Tag蛋白激活验证使用Human BAFF Protein; His Tag蛋白激活后，在使用Anti-BAFF hlgG1 Antibody(belimumab)抗体Block验证结果 GM-C24849:H_BCMA CHO-K1 Cell Line 使用Anti-BCMA hIgG1 Antibody(Belantamab) 抗体流式验证结果 GM-C24896:H_BCMA HEK-293 Cell Line 使用Anti-BCMA hIgG1 Antibody(Belantamab) 抗体流式验证结果 GM-C24899:Cynomolgus_BCMA CHO-K1 Cell Line 使用Anti-BCMA hIgG1 Antibody(Belantamab) 抗体流式验证结果联系我们吉满生物助力药物研发，紧随前沿靶点资讯，储备几百株现货细胞，覆盖GPCR、细胞因子、免疫检查点、TAA等多领域，截止当前已布局近500个热门靶向药靶点，1000余株细胞系，旨在助力、加速大分子早期研发，做到进口细胞的国产替代。同时可根据客户需求提供细胞系服务。扫码咨询扫码找现货

ASH会议临床1期上市批准临床结果引进/卖出

100 项与 Vera Therapeutics, Inc. 相关的药物交易

登录后查看更多信息

100 项与 Vera Therapeutics, Inc. 相关的转化医学

登录后查看更多信息