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Livedo Racemosa

Livedo Racemosa is a distinct dermatological condition characterized by persistent, broken, and irregular net-like (racemose) vascular patterns on the skin, which do not disappear with warming. Protheragen provides end-to-end preclinical drug and therapeutic development services for livedo racemosa, accelerating advancement of your research project.

Overview of Livedo Racemosa

Livedo Racemosa is a rare vascular disorder characterized by irregular, broken circular skin patterns signaling thrombotic vasculopathy or autoimmune dysregulation. With 60-70% association with antiphospholipid syndrome (APS) or vasculitis, LR requires urgent diagnostic intervention. Recent studies reveal HLA-DRB1 polymorphisms and impaired protein C pathway activation as key drivers.

The skin pattern of livedo reticularis and livedo racemosa.

Fig.1 Skin pattern of livedo reticularis and livedo racemosa. (Hartig, F., et al., 2020)

Pathogenesis of Livedo Racemosa

The pathogenesis of Livedo Racemosa primarily involves microvascular occlusion within the dermal and subcutaneous arterial plexuses. This occlusion leads to chronic tissue ischemia and hypoxia, manifesting as the characteristic persistent, branching violaceous discoloration.

Vascular Occlusion: The core mechanism involves partial or complete blockage of small to medium-sized arterioles. This can result from microthrombi (e.g., in antiphospholipid syndrome, polycythemia vera), vessel wall inflammation (vasculitis), intimal proliferation (e.g., Sneddon's syndrome), or cholesterol emboli.

Impaired Blood Flow: The compromised blood flow leads to deoxygenation of blood in the venules draining the affected areas, contributing to the distinct livedoid pattern. Unlike Livedo Reticularis, this pattern is fixed and does not blanch or disappear with warmth, indicating structural vascular changes.

Underlying Systemic Causes: The dermatological presentation often mirrors systemic pathological processes. Autoimmune conditions, hematological disorders, certain drug reactions, and infectious diseases can trigger the microvascular events that culminate in Livedo Racemosa.

Therapeutics Development for Livedo Racemosa

Therapeutic Strategy	Target / Intervention	Mechanistic Validation/Model Data	Development Stage
IVIG	Autoantibody neutralization, complement inhibition	Reduces C5a-induced endothelial activation in 3D microvascular models	Clinical use
Baricitinib	JAK1/2 inhibition (IFN-γ/STAT1 blockade)	Normalizes CXCL10/IP-10 in HLA-DRB1⁺ endothelial cells	Case reports
Eculizumab	C5 inhibitor (prevents MAC formation)	Blocks C5b-9 deposition in thrombotic microangiopathy models	Off-label use
Iloprost	Prostacyclin analog (vasodilation)	Restores capillary perfusion in cold-challenge organoids	Phase II
Imsidolimab	IL-36R antagonism	Suppresses IL-36-driven neutrophil extracellular traps (NETs) in vasculitis models	Phase II
Anifrolumab	IFNAR blockade	Abolishes type I IFN signature in SLE-associated LR endothelial cells	Phase I
ADSCs	VEGF/TSG-6-mediated endothelial repair	Reverses cholesterol emboli-induced vaso-occlusion in xenografts	Phase I/II
Nano-delivered Protein C	Targeted anticoagulant delivery	Localized thrombus resolution in microfluidic thrombosis-on-chip platforms	Preclinical

Disclaimer: Protheragen focuses on providing preclinical research services. This table is for information exchange purposes only. This table is not a treatment plan recommendation. For guidance on treatment options, please visit a regular hospital.

Our Services

Protheragen offers comprehensive services to advance therapeutics for Livedo Racemosa. Our team of expert scientists, dermatologists, and vascular specialists integrates specialized knowledge with advanced technologies to support your project through tailored therapeutic development and disease model development.

Therapeutic Development Platforms for Livedo Racemosa

Disease Models Development for Livedo Racemosa

Protheragen provides validated preclinical models to accelerate Livedo Racemosa research, including advanced 2D cell models, 3D skin models, and pathophysiology-relevant animal models.

2D Cell Models& 3D Skin Models

Autoantibody-Exposed Endothelial Cells
APS Patient-Derived Monocytes
Thrombosis-Primed Vascular Cell Co-cultures
Vascular-Skin Interface Organoids

Animal Models Development

β2GPI Immunization-Induced APS Murine Models
FcγRIIa-Transgenic Thrombosis Models
Complement Factor Mutant Mice (C3/C5)
Vascular Endothelial-Specific Knockouts

Drug Safety Evaluation & DMPK Services for Livedo Racemosa

In Vitro ADME Services

Endothelial Binding Assay
Plasma Protein Binding
Metabolic Stability
Anticoagulant Interaction
Vascular Permeability

In Vivo Pharmacokinetics Services

Skin Capillary Flow
Tissue Distribution
Thrombus Penetration
Blood-to-Plasma Ratio
Metabolite Profiling

Drug Safety Evaluation

As a one-stop preclinical research partner, Protheragen accelerates therapy development for rare skin diseases like livedo reticularis. We provide end-to-end solutions—from target discovery and disease modeling to drug safety evaluation and DMPK services. If you are interested in our services, please feel free to contact us.

References

Hartig, F., et al. "Livedo Racemosa - the Pathophysiology of Decompression-Associated Cutis Marmorata and Right/Left Shunt." Front Physiol 11 (2020): 994.
Mitri, F., et al. "Livedo Racemosa in Neurological Diseases: An Update on the Differential Diagnoses." Eur J Neurol 27.10 (2020): 1832-43.

All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.