Human IgG4 (PE) — IgG4-Stabilized & Effector-Silenced Isotype Vector

Human IgG4 (PE) — IgG4-Stabilized & Effector-Silenced Isotype Vector

$680.00

Plasmid Name: pHCIgG4PE(S228P/L235E)

Backbone: Human IgG4 heavy chain expression vector

Mutation Set: S228P (Core Hinge) + L235E (Lower Hinge)

Effector Profile: Fully Null / Ultra-Silent

Combines core hinge stabilization (S228P) to eliminate Fab-arm exchange with lower hinge substitution (L235E) to abolish residual FcγRI (CD64) binding. Provides a clinically validated, ultra-silent IgG4 backbone with normal FcRn recycling and half-life.

Plasmid Name
pHCIgG4PE(S228P/L235E)
Mutation Set
S228P (Core Hinge) + L235E (Lower Hinge)
Selection Marker
Ampicillin
Promoter
CMV

Fc Engineering Overview

Human IgG4 (PE) combines hinge stabilization (S228P) with lower-hinge silencing (L235E). While standard IgG4 (S228P) eliminates Fab-arm exchange, it retains residual affinity for FcγRI (CD64). The addition of L235E abolishes this residual binding, creating an ultra-silent IgG4 backbone that prevents both structural recombination and unwanted immune activation.

Functional Profile

Property Effect
Fab-Arm Exchange (in vivo) Completely Abolished (0%)
FcγRI (CD64) binding Completely Abolished ↓↓↓↓
FcγRII/III binding Undetectable
ADCC / ADCP Completely Null
C1q binding / CDC Undetectable
FcRn binding & recycling Unaltered / Normal Half-life

Mechanism of Action

S228P Substitution: Re-introduces the rigid CPPC motif into the core hinge, establishing permanent inter-heavy chain disulfide linkages and preventing half-antibody formation.
L235E Substitution: Introduces a negative charge and steric perturbation into the lower hinge region, disrupting the hydrophobic interaction required for high-affinity FcγRI (CD64) engagement without affecting FcRn endosomal recycling loops.

Phenotypic Effects

  • Complete protection against in vivo Fab-arm exchange and dynamic exchange with host IgGs.
  • Elimination of residual FcγRI-mediated monocyte/macrophage activation and cytokine release.
  • Zero detectable NK cell-mediated ADCC or macrophage-mediated ADCP.
  • Total absence of complement activation or C1q binding.
  • Maintains full serum half-life via intact FcRn interactions.
  • High structural integrity and batch homogeneity during recombinant mammalian expression.

Applications

  • Safety-critical therapeutic antibodies where complete elimination of FcγRI binding on an IgG4 framework is required.
  • Receptor-targeted antagonist or neutralizer antibodies where Fc-mediated receptor cross-linking or target-cell destruction must be completely avoided.
  • Immune checkpoint modulators targeting immune cells sensitive to FcγR-mediated hyper-activation.

Sequence Map & Feature Annotation

Insert Architecture: VH – CH1 – hinge(S228P) – lower hinge(L235E) - CH2(WT) – CH3(WT)

  • VH: Variable heavy domain
  • CH1: Constant heavy 1
  • Hinge(S228P): Stabilized IgG4 core hinge region (CPPC)
  • Lower Hinge(L235E): Effector-silencing lower hinge substitution
  • CH2: Constant heavy 2 (WT)
  • CH3: Constant heavy 3 (WT)

Product Note: The human IgG4 (PE) backbone is widely utilized in therapeutic development as a reinforced alternative to wild-type IgG4 or single-mutant IgG4 (S228P). By addressing both inter-chain disulfide stability and residual FcγRI engagement, it delivers a clinically validated, ultra-silent profile.

Storage & Handling

Plasmid: Store at −20 °C
Purified antibody:

  • 2–8 °C for short-term storage
  • −80 °C for long-term storage
  • Avoid repeated freeze–thaw cycles
  • Use sterile technique for all handling
  • Optimized for transient or stable expression in mammalian expression systems (CHO, HEK293)

References

  1. Alegre ML, Collins AM, Pulito VL, Brosius RA, Olson WC, Zivin RA, Knowles R, Thistlethwaite JR, Jolliffe LK, Bluestone JA. Effect of a single amino acid mutation on the activating and immunosuppressive properties of a “humanized” OKT3 monoclonal antibody. J Immunol. 1992; 148(11):3461-3468.
  2. Reddy MP, Kinney CA, Chaikin MA, Payne A, Fishman-Lobell J, Tsui P, Dal Monte PR, Doyle ML, Brigham-Burke MR, Anderson D, Reff M, Newman R, Hanna N, Sweet RW, Truneh A. Elimination of Fc receptor-dependent effector functions of a modified IgG4 monoclonal antibody to human CD4. J Immunol. 2000;164(4):1925-1933.