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Description

Chlorophyllin is a water soluble derivative of chlorophyll. It has chemopreventive properties and forms a non-covalent complex with many mutagenic/carcinogenic molecules. Chlorophyllin inhibits cancer initiation and progression by targeting multiple molecules and pathways involved in the metabolism of carcinogens, cell cycle progression, apoptosis evasion, invasion, and angiogenesis. The modulatory effects of Chlorophyllin to be mediated via abrogation of key oncogenic signal transduction pathways such as nuclear factor kappa B, Wnt/β-catenin, and phosphatidylinositol-3-kinase/Akt signaling. Chlorophyllin sodium copper salt mitigates radiation-induced hematopoietic syndrome by increasing the abundance of hematopoietic stem cells, enhancing granulopoiesis, and stimulating prosurvival pathways in bone marrow cells and lymphocytes. In addition, chlorophyllin exhibits antioxidant, antiapoptotic and immunostimulatory effects. Chlorophyllin is intended to improve the quality of life in people who have fecal incontinence due to spinal cord injury, bowel cancer, psychotic disorder, terminal illness, or other disorders. Chlorophyllin is also used by people who have had a colostomy or ileostomy

CNS Activity

Approval Year

Targets

Primary TargetPharmacologyConditionPotency

Conditions

ConditionModalityTargetsHighest PhaseProduct
Palliative
Unknown
Primary
Unknown
Palliative
Derifil

Doses

PubMed

Sample Use Guides

In Vivo Use Guide
urinary odor: each patient received chlorophyllin 100 mg/d for two weeks and placebo daily for two weeks, separated by a washout period of one week.
Route of Administration: Oral
In Vitro Use Guide
It was investigated the effects on cell proliferation and the expression of genes involved in apoptosis, and the cell cycle in HB4a cells treated with Chlorophyllin (Chl). Chl was cytotoxic and induced apoptosis to HB4a cells at 400 μg/mL. Analysis of gene expression showed that there was a decrease in the mRNA level of BIRC5 and CCNA2 genes involved in apoptosis and cell cycle progression, respectively. The proapoptotic gene BAX and the antiapoptotic genes BCL-2 and BCL-XL were upregulated. The cytotoxicity of Chl has been attributed to increases in the expression of BAX and decreases in the expression of genes involved in the cell cycle, but increases in the expression of anti-apoptotic genes suggests a mechanism for protection from cell death induced by Chl.
Substance Class Mixture
Record UNII
1D276TYV9O
Record Status Validated (UNII)
Record Version
All of the following components must be present:
Definition References
(2)