Table 1.

Gain-of-function FVIII variants

FVIII
variant
Gain of functionProtein changeFold
change
Reference
SQ High expression B domain replaced by 14 amino acid linker (Figure 1) with increased messenger RNA levels but decreased secretion efficiency 21  
N6 Increase secretion B domain replaced by 226 amino acid linker from the N-terminal of the B domain 29  
V3 Increase secretion Incorporation of 6 N-glycosylation sites within SQ- linker (Figure 1) 2-3 31  
ΔF  Increase secretion Removal of furin recognition motif from SQ-linker (Figure 1) 34  
Δ3-SP/DE  Increase secretion Partial removal of furin recognition motif from SQ-linker and elimination of secondary cleavage site in a3 (Figure 1) 2-5 35  
F309S Increase secretion Polar amino acid substitution in A1 hydrophobic patch 2.3 36  
L303E/F309S Increase secretion Polar amino acid substitutions in A1 hydrophobic patch 36  
ET3  Increase secretion Human/porcine hybrid 10 40  
X5  Increase secretion 5 porcine amino acid substitutions in A1 (V86I, S108A, K132G,
T147M, and P152L) 
41  
C1899G/C1903G Increase secretion 2 substitutions within A3 to eliminate a disulfide bond 1.5 65  
P290T High specific activity 1 amino acid substitution in A1 1.5 66  
K1813A High specific activity 1 amino acid substitution in A3 67  
K12  High specific activity 10 canine amino acid substitutions (V1857I, H1859R, M1907K, M1926K, L1975V, A1993V, H2007Q, D2066E, K2085M, and Q2113H) and 2 additional substitutions (S2157N and R2159H) in the light chain 68  
IR8 Inactivation resistant B domain replaced by 54 amino acid linker from the N-terminal; a3 removed; R336I and R562K to limit APC inactivation; R740A to limit thrombin cleavage 69  
CC Inactivation resistant 2 substitutions (Y664C/T1826C) or (M662C/D1828C) to introduce a disulfide bond between A2 and A3 70  
VV Inactivation resistant 2 hydrophobic substitutions for negative charge amino acids in the A2-domain (D519V and E665) 71  
QQ Inactivation resistant Elimination of both APC cleavage sites (R336Q and R562Q) 72  
FVIII
variant
Gain of functionProtein changeFold
change
Reference
SQ High expression B domain replaced by 14 amino acid linker (Figure 1) with increased messenger RNA levels but decreased secretion efficiency 21  
N6 Increase secretion B domain replaced by 226 amino acid linker from the N-terminal of the B domain 29  
V3 Increase secretion Incorporation of 6 N-glycosylation sites within SQ- linker (Figure 1) 2-3 31  
ΔF  Increase secretion Removal of furin recognition motif from SQ-linker (Figure 1) 34  
Δ3-SP/DE  Increase secretion Partial removal of furin recognition motif from SQ-linker and elimination of secondary cleavage site in a3 (Figure 1) 2-5 35  
F309S Increase secretion Polar amino acid substitution in A1 hydrophobic patch 2.3 36  
L303E/F309S Increase secretion Polar amino acid substitutions in A1 hydrophobic patch 36  
ET3  Increase secretion Human/porcine hybrid 10 40  
X5  Increase secretion 5 porcine amino acid substitutions in A1 (V86I, S108A, K132G,
T147M, and P152L) 
41  
C1899G/C1903G Increase secretion 2 substitutions within A3 to eliminate a disulfide bond 1.5 65  
P290T High specific activity 1 amino acid substitution in A1 1.5 66  
K1813A High specific activity 1 amino acid substitution in A3 67  
K12  High specific activity 10 canine amino acid substitutions (V1857I, H1859R, M1907K, M1926K, L1975V, A1993V, H2007Q, D2066E, K2085M, and Q2113H) and 2 additional substitutions (S2157N and R2159H) in the light chain 68  
IR8 Inactivation resistant B domain replaced by 54 amino acid linker from the N-terminal; a3 removed; R336I and R562K to limit APC inactivation; R740A to limit thrombin cleavage 69  
CC Inactivation resistant 2 substitutions (Y664C/T1826C) or (M662C/D1828C) to introduce a disulfide bond between A2 and A3 70  
VV Inactivation resistant 2 hydrophobic substitutions for negative charge amino acids in the A2-domain (D519V and E665) 71  
QQ Inactivation resistant Elimination of both APC cleavage sites (R336Q and R562Q) 72  

Variants highlighted in bold are included in rAAV vectors approved or in clinical trials.

Variants engineered based on FVIII orthologs

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