Citrus pectin: E440 additive, INCI functions, identifiers (CAS/EC), gelling properties, and formulation guidance

Citrus pectin
Citrus Pectin – polysaccharide (heteropolysaccharide) based on polygalacturonic acid (partially esterified)

Synonyms: pectin (citrus), pectin from citrus peel, E440(i) pectins (food use)
INCI / functions: binding, emulsion stabilising, film forming, viscosity controlling (typical cosmetic functions)

Definition
Citrus pectin is a polysaccharide extracted mainly from citrus peel (botanical matrices of the Rutaceae family), composed predominantly of galacturonic acid chains (a “polygalacturonic acid” backbone partially methyl-esterified). From a compositional standpoint, the ingredient corresponds to a polymeric mixture with variable degree of esterification: HM (high methoxyl) and LM (low methoxyl) pectins differ in gelling mechanism and use conditions. In food formulation, it is a reference gelling agent and thickener, while in cosmetics it is used to increase viscosity, stabilize dispersed systems, and contribute to a more film-forming and uniform skin feel.

Calories (energy value)

Identification data and specifications

Key constituents

Physicochemical properties (indicative)

Functional role and practical mechanism of action

Typical gelling conditions 

Formulation compatibility

In food applications, pectin performance depends critically on pH, soluble solids (sugars), calcium presence, and processing profile (temperature, shear, hydration time). In HM systems, efficiency increases with adequate acidity and sugar content; in LM systems, control of Ca²⁺ ions is essential (dose and form, to avoid overly rigid gels or localized precipitation).

In cosmetics, pectin is generally compatible with aqueous systems and O/W emulsions as a rheology modifier, but it can be sensitive to: (i) high electrolyte levels (viscosity changes), (ii) extreme pH, and (iii) interactions with cationic polymers (potential complexation). In “clear” formulas, achieving full transparency can be challenging: the outcome depends on dispersion quality and the selected grade. Good practice is to introduce pectin with proper wetting (premix with sugar in food, or with compatible humectants in cosmetics) to minimize lumps and “fish-eyes”.

Use guidelines (indicative)

Typical applications

• Food: gel formation (jams), stabilization of fruit preparations, texture improvement, and reduced syneresis in selected systems.

• Cosmetics: gels and masks requiring controlled viscosity, improved suspension stability, and support for a light sensorial film.

• Pharmaceutical/technical: use as a functional polymer (thickener/binder) in selected systems, depending on quality specifications.

Quality, grades and specifications

Safety, regulation and environment

In food, pectin is a well-established additive (category E440) used under the conditions applicable to the product category. In cosmetics, as a plant-derived polymer, the correct safety approach is the finished product assessment: attention to purity, contaminants, and microbiological stability in aqueous formulas. From an environmental perspective, it is a naturally derived substance; practical sustainability considerations are mainly linked to industrial handling of process water and organic residues in line with local regulation and good operational practice.

Formulation troubleshooting

Conclusion

Citrus pectin is a plant polymer based on polygalacturonic acid, primarily used as a gelling agent and thickener in food (E440) and as a rheology modifier in cosmetics. Selecting the appropriate grade (HM/LM), managing pH, sugars or Ca²⁺, and using a controlled hydration process are decisive for repeatable performance and long-term stability.

Studies

Anti-tumour activity and membrane permeability: Findings suggested that citrus PET-pectin can be developed as a potential dietary supplement in plant origin for cancer prevention (1).

This study aims to better understand the implications that chemical modifications may impose on the structure of citrus pectins (2).

The present study revealed that MCP, a galectin‑3 inhibitor, reduced the size of atherosclerotic lesions by inhibiting the adhesion of leucocytes to endothelial cells. Inhibition of galectin‑3 function may be a therapeutic strategy for the treatment of atherosclerosis (3).

Mini-glossary

References__________________________________________________________________________

(1) Huang, P.H., Fu, L.C., Huang, C.S., Wang, Y.T., and Wu, M.C. The uptake of oligogalacturonide and its effect on growth inhibition, lactate dehydrogenase activity and galactin-3 release of human cancer cells.  Food Chem. 2012; 132: 1987–1995

Abstract. Anti-tumour activity and membrane permeability of 1 kDa oligogalacturonide (PET-pectin), prepared from citrus pectin after 24 h hydrolysis, by commercial pectic enzyme produced by Aspergillus niger, on four human cell lines (HepG2, A549, Colo 205, and HEK293) and the uptake of oligogalacturonide by HEK293 cell and BALB/c mouse were investigated. PET-pectin causes a higher value of growth inhibition, lactate dehydrogenase release, and galactin-3 release in human cancer cells, as compared to the human normal HEK293 cell. There was a good correlation between growth inhibition of human cells and the uptake of rhodamine B-PET-pectin content by these cells. Additionally, almost no difference between growth inhibitions of human normal HEK293 cells cultivated with PET-pectin and pectin was found. Total pectin content in the blood of PET-pectin administrated mice increased to a maximum at 2 h after oral administration, while it did not increase and change in pectin administrated mice. Our findings suggested that citrus PET-pectin can be developed as a potential dietary supplement in plant origin for cancer prevention.

(2) Fracasso AF, Perussello CA, Carpiné D, Petkowicz CLO, Haminiuk CWI. Chemical modification of citrus pectin: Structural, physical and rheologial implications. Int J Biol Macromol. 2018 Apr 1;109:784-792. doi: 10.1016/j.ijbiomac.2017.11.060. Epub 2017 Nov 11.

(3) Lu Y, Zhang M, Zhao P, Jia M, Liu B, Jia Q, Guo J, Dou L, Li J. Modified citrus pectin inhibits galectin-3 function to reduce atherosclerotic lesions in apoE-deficient mice. Mol Med Rep. 2017 Jul;16(1):647-653. doi: 10.3892/mmr.2017.6646.

Abstract. Galectin-3 is a carbohydrate-binding lectin, which has been implicated in the modulation of atherosclerotic pathophysiology, and is highly expressed in monocytes, macrophages and endothelial cells within atherosclerotic plaques. Modified citrus pectin (MCP) is produced from citrus pectin via pH and temperature modifications, which break it into shorter, non‑branched, galactose‑rich carbohydrate chains. MCP is able to tightly bind with galectin‑3, via recognition of its carbohydrate recognition domain, and facilitates the modulation of galectin‑3‑induced bioactivity. The present study explored the effects of MCP on the initiation of atherosclerosis. Eight‑week‑old apolipoprotein E‑deficient mice were treated with 1% MCP and fed an atherogenic diet for 4 weeks. The effects of MCP on atherosclerotic initiation were determined by pathological analysis and scanning electron microscope (SEM) imaging. MCP treatment reduced the size of atherosclerotic lesion areas, which was accompanied by decreased numbers of macrophages and smooth muscle cells (SMCs). Furthermore, SEM examination of the surface of the atheroma‑prone vessel wall indicated that MCP treatment reduced endothelial injury. To analyze the effects of MCP on monocyte adhesion, firstly, oxidized‑low density lipoprotein and various concentrations of MCP (0.025, 0.05, 0.1 and 0.25%) were incubated with the human umbilical vein endothelial cells (HUVECs) for stimulation and following this, the U937 cells were plated onto the HUVECs. The results revealed that MCP reduced the adhesion of U937 monocytes to HUVECs, indicating the adhesion-inhibiting effects of MCP. In conclusion, the present study revealed that MCP, a galectin‑3 inhibitor, reduced the size of atherosclerotic lesions by inhibiting the adhesion of leucocytes to endothelial cells. Inhibition of galectin‑3 function may be a therapeutic strategy for the treatment of atherosclerosis.