Ig Uniquely Covers the Complexities of CIDP^1-3

CIDP is a complex disease with multiple underlying drivers, all of which may contribute to a
pro-inflammatory environment^4-9

These drivers can include:

T-cells reduction impairs the ability to regulate autoreactive cells, inflammation, and immune homeostasis

B cells can differentiate into plasma cells that release autoantibodies

Pathogenic antibodies contribute to demyelination and axonal damage

Complement activation assoicated with macrophagemediated demyelination

Ig works beyond FcRn antagonism alone^3,9*

Pathogenic mechanisms of CIDP	Mechanisms of Ig^8-14
Pathogenic mechanisms of CIDP	Complement antagonism	T cell (Tregs) increase	FcγR antagonism	Neutralization via Fab	FcRn antagonism
T cell (Tregs) reduction
B cell production of autoantibodies
Pathogenic antibodies
Complement activation

Mechanisms of Ig^8-14	Pathogenic mechanisms of CIDP
Mechanisms of Ig^8-14	T cell (Tregs) reduction	B cell production of autoantibodies	Pathogenic antibodies	Complement activation
Complement antagonism
T cell (Tregs) increase
FcγR antagonism
Neutralization via Fab
FcRn antagonism

Differences in the clinical presentation of CIDP and a wide range of responses suggest a variety of mechanisms are at play.¹⁵

Ig activity involves both the Fc Constant Region and the Fab Variable Regions. By inducing a range of mechanisms thought to help inhibit and block the pathogenic effects of demyelination, Ig therapy reduces or prevents further nerve damage without suppressing the immune system.^5,9

*The mechanisms of action have not been fully elucidated, but may include immunomodulatory effects.

CIDP=chronic inflammatory demyelinating polyneuropthy;

Fab=fragment antigen-binding; Fc=fragment crystallizable;

FcyR=Fc gamma receptor; FcRn=neonatal Fc receptor; Tregs=T regulatory cells.

Understanding Immunoglobulin G (IgG), also commonly referred to as Ig

Watch this video to explore the proposed mechanism of action of Ig^*

*HIZENTRA supplies a broad spectrum of opsonizing and neutralizing IgG antibodies against a wide variety of bacterial and viral agents.
The mechanism of action of Ig has not been fully elucidated, but may include immunomodulatory effects.

Explore how Hizentra may be right for your CIDP patients

See the benefits

Consider the profiles of patients who could benefit

Optimize the Ig experience

References: 1. Berger M, McCallus DE, Lin CS. Rapid and reversible responses to IVIG in autoimmune neuromuscular diseases suggest mechanisms of action involving competition with functionally important antibodies. J Peripher Nerv Syst. 2013;18(4):275-296. 2. Sevim E, Kobrin D, Casal-Dominguez M, Pinal-Fernandez I. A comprehensive review of dermatomyositis treatments – from rediscovered classics to promising horizons. Expert Rev Clin Immunol. 2024;20(2):197-209. 3. Dalakas MC, Latov N, Kuitwaard K. Intravenous immunoglobulin in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): mechanisms of action and clinical and genetic considerations. Expert Rev Neurother. 2022;22(11-12):953-962. 4. Dalakas MC. Advances in the diagnosis, pathogenesis and treatment of CIDP. Nat Rev Neurol. 2011;7(9):507-517. 5. Querol L, Lleixà C. Novel immunological and therapeutic insights in Guillain-Barré Syndrome and CIDP. Neurotherapeutics. 2021;18(4):2222-2235. 6. Querol LA, Hartung HP, Lewis RA, et al. The Role of the Complement System in Chronic Inflammatory Demyelinating Polyneuropathy: Implications for Complement-Targeted Therapies. Neurotherapeutics. 2022;19(3):864-873. 7. Goswami TK, Singh M, Dhawan M, et al. Regulatory T cells (Tregs) and their therapeutic potential against autoimmune disorders - Advances and challenges. Hum Vaccin Immunother. 2022;18(1):2035117. 8. Tackenberg B, Nimmerjahn F, Lünemann JD. Mechanisms of IVIG efficacy in chronic inflammatory demyelinating polyneuropathy. J Clin Immunol. 2010;30 Suppl 1:S65-S69. 9. Schwab I, Nimmerjahn F. Intravenous immunoglobulin therapy: how does IgG modulate the immune system? Nat Rev Immunol. 2013;13(3):176-189. 10. Trinath J, Hegde P, Sharma M, et al. Intravenous immunoglobulin expands regulatory T cells via induction of cyclooxygenase-2-dependent prostaglandin E2 in human dendritic cells. Blood. 2013;122(8):1419-1427. 11. Lutz HU, Späth PJ. Anti-inflammatory effect of intravenous immunoglobulin mediated through modulation of complement activation. Clin Rev Allergy Immunol. 2005;29(3):207-212. 12. Dalakas MC. Update on Intravenous Immunoglobulin in Neurology: Modulating Neuro-autoimmunity, Evolving Factors on Efficacy and Dosing and Challenges on Stopping Chronic IVIg Therapy. Neurotherapeutics. 2021;18(4):2397-2418. 13. Ritter C, Bobylev I, Lehmann HC. Chronic inflammatory demyelinating polyneuropathy (CIDP): change of serum IgG dimer levels during treatment with intravenous immunoglobulins. J Neuroinflammation. 2015;12:148. 14. Allen JA, Berger M, Querol L, Kuitwaard K, Hadden RD. Individualized immunoglobulin therapy in chronic immune-mediated peripheral neuropathies. J Peripher Nerv Syst. 2018;23(2):78-87. 15. Mathey EK, Park SB, Hughes RA, et al. Chronic inflammatory demyelinating polyradiculoneuropathy: from pathology to phenotype. J Neurol Neurosurg Psychiatry. 2015;86(9):973-985.

Ig Uniquely Covers the Complexities of CIDP1-3

These drivers can include:

Ig works beyond FcRn antagonism alone3,9*

Pathogenic mechanisms of CIDP

Mechanisms of Ig8-14