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CFB

Official Full Name
complement factor B
Organism
Homo sapiens
GeneID
629
Background
This gene encodes complement factor B, a component of the alternative pathway of complement activation. Factor B circulates in the blood as a single chain polypeptide. Upon activation of the alternative pathway, it is cleaved by complement factor D yielding the noncatalytic chain Ba and the catalytic subunit Bb. The active subunit Bb is a serine protease which associates with C3b to form the alternative pathway C3 convertase. Bb is involved in the proliferation of preactivated B lymphocytes, while Ba inhibits their proliferation. This gene localizes to the major histocompatibility complex (MHC) class III region on chromosome 6. This cluster includes several genes involved in regulation of the immune reaction. Polymorphisms in this gene are associated with a reduced risk of age-related macular degeneration. The polyadenylation site of this gene is 421 bp from the 5' end of the gene for complement component 2. [provided by RefSeq, Jul 2008]
Synonyms
BF; FB; BFD; GBG; CFAB; CFBD; PBF2; AHUS4; FBI12; H2-Bf; ARMD14;
Bio Chemical Class
mRNA target
Protein Sequence
MGSNLSPQLCLMPFILGLLSGGVTTTPWSLARPQGSCSLEGVEIKGGSFRLLQEGQALEYVCPSGFYPYPVQTRTCRSTGSWSTLKTQDQKTVRKAECRAIHCPRPHDFENGEYWPRSPYYNVSDEISFHCYDGYTLRGSANRTCQVNGRWSGQTAICDNGAGYCSNPGIPIGTRKVGSQYRLEDSVTYHCSRGLTLRGSQRRTCQEGGSWSGTEPSCQDSFMYDTPQEVAEAFLSSLTETIEGVDAEDGHGPGEQQKRKIVLDPSGSMNIYLVLDGSDSIGASNFTGAKKCLVNLIEKVASYGVKPRYGLVTYATYPKIWVKVSEADSSNADWVTKQLNEINYEDHKLKSGTNTKKALQAVYSMMSWPDDVPPEGWNRTRHVIILMTDGLHNMGGDPITVIDEIRDLLYIGKDRKNPREDYLDVYVFGVGPLVNQVNINALASKKDNEQHVFKVKDMENLEDVFYQMIDESQSLSLCGMVWEHRKGTDYHKQPWQAKISVIRPSKGHESCMGAVVSEYFVLTAAHCFTVDDKEHSIKVSVGGEKRDLEIEVVLFHPNYNINGKKEAGIPEFYDYDVALIKLKNKLKYGQTIRPICLPCTEGTTRALRLPPTTTCQQQKEELLPAQDIKALFVSEEEKKLTRKEVYIKNGDKKGSCERDAQYAPGYDKVKDISEVVTPRFLCTGGVSPYADPNTCRGDSGGPLIVHKRSRFIQVGVISWGVVDVCKNQKRQKQVPAHARDFHINLFQVLPWLKEKLQDEDLGFL
Open
Disease
Urinary system clinical sympton
Approved Drug
1 +
Clinical Trial Drug
4 +
Discontinued Drug
1 +

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Detailed Information

Complement Factor B (CFB) is a key component of the alternative pathway (AP) of the complement system. The CFB gene is located on chromosome 6p21.3, within the MHC class III region, and is tightly linked to other complement-related genes such as C2 and C4. It encodes a 93-kDa serine protease that comprises four distinct structural domains: a complement control protein (CCP) domain, an epidermal growth factor (EGF)-like domain, a von Willebrand factor type A (VWFA) domain, and a serine protease domain.

CFB expression is tightly regulated by inflammatory signals. Transcription factors such as NF-κB and AP-1 bind to the promoter region of the CFB gene, markedly increasing its transcription—up to three- to five-fold—upon stimulation by inflammatory mediators such as TNF-α or lipopolysaccharide (LPS).

Importantly, there are two functionally distinct haplotypes of the CFB gene: H1 and H2. The H1 haplotype, tagged by the SNP rs4151657, is associated with elevated serum CFB levels and confers a 2.3-fold increased risk of age-related macular degeneration (AMD).

Figure 1. Overview of the three complement activation pathways—classical, lectin, and alternative—and their regulation by complement inhibitors and receptors.Figure 1. Overview of the three complement activation pathways—classical, lectin, and alternative—and their regulation by complement inhibitors and receptors. (Kavanagh D, et al., 2025)

Biological Functions and Pathogenic Mechanisms

CFB plays a central role in the amplification loop of the alternative complement pathway, participating in both immune defense and tissue injury under pathological conditions.

1. Complement Cascade Activation

Upon binding to C3b, CFB is cleaved by Factor D (CFD) into Ba and Bb fragments. The Bb fragment, in complex with C3b, forms the C3 convertase (C3bBb), which catalyzes the cleavage of additional C3 molecules. This leads to the generation of downstream effectors such as C3a, C5a, and the membrane attack complex (MAC). While essential for pathogen elimination, uncontrolled activation can contribute to inflammatory tissue damage.

2. Immunometabolic Crosstalk

In diabetic peripheral neuropathy (DPN), chronic hyperglycemia drives pathological CFB expression via multiple mechanisms:

  • Increased mitochondrial reactive oxygen species (mtROS) activate the NF-κB pathway.
  • Accumulation of advanced glycation end-products (AGEs) and interaction with RAGE further enhance CFB transcription.

Clinical studies have shown that serum CFB levels in DPN patients average 845.43 ± 101.10 μg/mL, significantly higher than levels in patients with uncomplicated diabetes (792.19 ± 116.59 μg/mL) and healthy individuals (739.20 ± 123.43 μg/mL).

3. Tissue-Specific Mechanisms of Injury

  • Neuropathy: CFB-mediated generation of C5a contributes to Schwann cell apoptosis and disruption of the blood-nerve barrier, leading to impaired nerve conduction.
  • Retinal Degeneration: Aberrant expression of CFB in retinal pigment epithelial (RPE) cells promotes MAC deposition, contributing to choroidal neovascularization in AMD.
  • Atherosclerosis: Upregulated CFB in vascular endothelial cells promotes monocyte adhesion, enhancing foam cell formation and plaque progression.

Clinical Relevance and Translational Applications

Therapeutic strategies targeting CFB have demonstrated promise in several chronic inflammatory diseases:

  • Monoclonal Antibodies: Anti-CFB antibody MIV-711 significantly reduced levels of the cartilage degradation biomarker CTX-I in a Phase II trial for osteoarthritis, with a 45% decrease compared to placebo.
  • Small-Molecule Inhibitors: Oral CFB inhibitor LNP023 (also known as iptacopan) has shown clinical benefit in patients with paroxysmal nocturnal hemoglobinuria (PNH), with 54% achieving transfusion independence.
  • Metabolic Interventions: In DPN, SGLT2 inhibitors have been found to reduce both HbA1c and oxidative stress, leading to an 18.7% decrease in serum CFB levels.

Challenges and Future Directions

A major limitation of CFB-targeted therapy is the increased risk of infections, particularly by encapsulated bacteria such as Streptococcus pneumoniae. This arises from the dampening of the alternative pathway, a critical component of innate immunity. Mitigation strategies include:

  • Development of tissue-targeted delivery systems, such as intraocular sustained-release implants.
  • Implementation of preventive vaccination, for example, pneumococcal polysaccharide vaccines.

Another emerging concern is complement pathway compensation. Inhibiting CFB may inadvertently enhance classical pathway activity, necessitating dual-pathway inhibition strategies. Agents targeting upstream components like C3 are currently under investigation.

Multi-omics-guided CFB genotyping may advance the precision medicine landscape. Individuals carrying the high-risk H1 haplotype could benefit from early-stage intervention, paving the way for personalized complement modulation therapies.

Reference

  1. Kavanagh D, Barratt J, Schubart A, et al. Factor B as a therapeutic target for the treatment of complement-mediated diseases. Front Immunol. 2025 Feb 14;16:1537974.

  2. Xu B, Kang B, Chen J, et al. Factor B inhibitor iptacopan for the treatment of paroxysmal nocturnal hemoglobinuria. Blood Rev. 2024 Jul;66:101210.

  3. Kavanagh D, Barratt J, Schubart A, et al. Factor B as a therapeutic target for the treatment of complement-mediated diseases. Front Immunol. 2025 Feb 14;16:1537974.

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