Database for
Therapeutic Antibodies
Therapeutic Antibodies
| Entry ID | 302 |
| INN | None |
| Status | Clinical |
| Drug code(s) | ANX005 |
| Brand name | None |
| mAb sequence source | mAb humanized |
| General Molecular Category | Naked monospecific |
| Format, general category | Full length Ab |
| Format details | None |
| Isotype (Fc) | IgG4 |
| Light chain isotype | kappa |
| Linker | None |
| Ave. DAR | None |
| Conjugated/fused moiety | None |
| Discovery method/technology | None |
| Target(s) | Complement C1q |
| Indications of clinical studies | Guillain-Barré Syndrome, Warm Autoimmune Hemolytic Anemia, Huntington Disease, Amyotrophic Lateral Sclerosis, Phase 1 in healthy volunteers |
| Primary therapeutic area | Neurological disorders |
| Most advanced stage of development (global) | Phase 3 |
| Status | Active |
| Start of clinical phase (IND filing or first Phase 1) | December 15, 2016 |
| Start of Phase 2 | August 17, 2020 |
| Start of Phase 3 | December 15, 2020 |
| Date BLA/NDA submitted to FDA | |
| Year of first approval (global) | None |
| Date of first US approval | |
| INN, US product name | None |
| US or EU approved indications | None |
| Company | Annexon Inc. |
| Licensee/Partner | None |
| Comments about company or candidate | June 2024: BLA submission are expected in the first half of 2025. Annexon plans to present Phase 3 data at the 2024 Peripheral Nerve Society Annual Meeting on June 25, 2024. https://ir.annexonbio.com/news-releases/news-release-details/annexon-announces-positive-topline-results-pivotal-phase-3-trial Phase 3 study for Guillain-Barré syndrome (NCT04701164) is recruiting as of March 9, 2023 As of Jan 2023, Annexon has prioritized resources and execution of late-stage development of its flagship programs: Guillain-Barré syndrome (GBS), Huntington’s disease (HD), geographic atrophy July 2022: Still listed as Phase 2/3 in G-B syndrome in corporate presentation; data expected in 2023. Phase 2 for Huntington's disease and ALS Dec 21, 2020: Annexon, Inc, a clinical stage biopharmaceutical company developing novel therapies for patients with classical complement-mediated disorders of the brain, body, and eye, announced that patient dosing has started in a Phase 2/3 clinical study (NCT04701164) of full-length monoclonal antibody, ANX005, to treat Guillain-Barré Syndrome (GBS). Annexon has completed a Phase 1b monotherapy clinical trial of ANX005 in GBS and has received Fast Track and Orphan Drug designations from the U.S. Food and Drug Administration for the treatment of GBS. NCT04691570 Phase 2 study in Warm Autoimmune Hemolytic Anemia not yet recruiting when first posted on Dec 31, 2020. NCT04569435 Phase 2 in Amyotrophic Lateral Sclerosis not yet recruiting when first posted on Sep 29 2020. NCT04035135 Phase 1/2 in GBS started in Jan 2020. Sep 2019: FDA granted fast track designation to Annexon Biosciences' investigational candidate ANX005 as a treatment for the autoimmune disease Guillain-Barre syndrome. Annexon has completed its Phase Ib trial for ANX005 and plans to launch later-stage studies. Phase 1 NCT03010046 study, as of June 2018, terminated (ANX005 well tolerated at doses studied; study discontinued and initiated in patient population) |
| Full address of company | 1400 Sierra Point Parkway, Building C, 2nd Floor, Brisbane, CA 94005 North America United States of America https://annexonbio.com/ |
Produced in CHO cells. Nonclinical Development of ANX005: A Humanized Anti-C1q Antibody for Treatment of Autoimmune and Neurodegenerative Diseases (http://journals.sagepub.com/doi/10.1177/1091581817740873). Dec 2016 ASH abstract 1265 ANX005, an Inhibitory Antibody Against C1q, Blocks Complement Activation Triggered By Cold Agglutinins in Human Disease: Humanized monoclonal antibody (ANX005) binds with high-affinity (~10 pM) to C1q and blocks classical complement activation & hemolysis in an in vitro sheep RBC assay. We evaluated the impact of ANX005 on hemolysis and complement deposition on human RBCs that were pre-sensitized with sera from CAD subjects. ANX005 showed a dose-dependent reduction in hemolysis using both individual and pooled CAD sera as the source of cold agglutinin. We further demonstrated that C1q blockade led to a robust reduction in C4 and C3 fragment deposition onto human RBCs. These results demonstrate that C1q inhibition is an effective way to impede C4 and C3 activation and downstream assembly of the lytic complex in sera from CAD patients, and support the clinical development of ANX005 in CAD and other antibody-mediated diseases
| Anticipated events | BLA submission are expected in the first half of 2025 |
| Factor(s) contributing to discontinuation | None |