Target intelligence / Profile preview

Complement factor H-related protein 2 (CFHR2)

Target
CFHR2
Molecular classification
Other (member of the factor H protein family, soluble regulatory glycoprotein)
01

Overview

Complement factor H-related protein 2 (CFHR2) is a soluble glycoprotein synthesized in the liver and secreted into plasma, part of the factor H protein family involved in complement regulation. CFHR2 is composed of four short consensus repeat domains (SCRs), and functions principally by binding to C3b and inhibiting the alternative pathway C3 convertase and the assembly of the terminal complement complex. CFHR2 forms homodimers which show avidity for tissue-bound complement complexes; unlike factor H, CFHR2 does not have decay accelerating or cofactor activity for factor I but instead directly inhibits substrate cleavage by the C3 convertase. CFHR2 mutations or deletions are associated with complement-related pathologies including dense deposit disease, age-related macular degeneration, and glomerulonephritis. CFHR2 is not currently a direct target of any approved drugs, but it is functionally relevant in the development of therapies targeting the complement system[1][2][3][4].

Other names
Complement factor H-related protein 2CFHR2CFHL2FHR2HFL3FHR-2DDESK59H factor-like 3H factor-like protein 2factor H-related gene 2
02

Mechanism of action

For hypothetical drugs: inhibition of alternative complement pathway, blockade of C3 convertase activity, or inhibition of terminal complement complex assembly[1][2]

03

Biological functions

Complement regulationInhibition of the alternative pathway C3 convertaseInhibition of the terminal complement complex assemblyImmune response modulationPossible role in lipid metabolism[3][4]
04

Disease associations

InflammationGlomerulonephritis (complement-mediated nephropathies)Dense deposit diseaseAge-related macular degeneration[1][2]Other
05

Safety considerations

Possible risks from systemic complement inhibition (e.g., increased susceptibility to infection, off-target effects on homeostasis)Genetic deletion/mutation may result in loss of complement regulation and tissue injury[1][2]
06

Biomarkers

Disease-associated CFHR2 mutations/deletions for dense deposit disease, CFHR nephropathy, age-related macular degeneration[1][2]

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