Nomilin: A Comprehensive Reference
1. Identity, Chemical Nature, and Natural Sources
Nomilin is one of the major limonoids, which are plant secondary metabolites also known as tetranortriterpenoids. Limonoids, first reported in 1864, are a group of chemically related triterpene derivatives found in the Rutaceae and Meliaceae families. Limonoids are highly oxygenated modified triterpenes that are biosynthesized from the acetate–mevalonate pathway in citrus fruits.
Nomilin has the molecular formula C28H34O9 and contains a dilactone structure and a furan ring attached to the closed D-ring at C-17. Citrus limonoids are comprised of two nucleus structures: the first general nucleus consists of five rings, while the second structure is composed of four rings designated as A, B, C, and D. The structure of nomilin exemplifies the second general nucleus. The structural features of nomilin-type limonoids are similar to limonin-type, except for ring A, which is a seven-membered lactone with the oxygen atom positioned between C-3 and C-4.
The name "nomilin" reflects the compound's close structural kinship with limonin. Since this substance is closely associated with limonin and similar in chemical properties to it, the name "nomilin" was proposed. For most Citrus species, limonin is the most abundant aglycone, followed by nomilin, and limonin glucoside is the most representative limonoid glucoside.
1.1 Botanical Sources
Nomilin is found mostly in common edible citrus fruits including lemons, limes, oranges, grapefruits, and mandarins, along with traditional Chinese medicines derived from citrus fruits, such as tangerine seed, tangerine peel, and fructus aurantii immaturus. Limonoids occur in significant amounts as aglycones and glycosides in seeds and fruit tissues. Citrus fruits contain approximately 36 limonoid aglycones and 17 limonoid glucosides.
Lemon seeds are among the most abundant sources of limonoids, with nomilin present alongside obacunone, ichangin, and deacetylnomilin. Sites of limonoid biosynthesis have been located in Citrus limon; the stem was found to be the major site of nomilin biosynthesis from acetate.
1.2 Occurrence as Aglycone and Glucoside
Limonoids can be present as water-soluble "tasteless" glucosides and as water-insoluble "bitter" aglycones. Limonin-17β-d-glucopyranoside is the most common glucoside, while limonin and nomilin are the most abundant aglycones, and both are responsible for the bitterness of citrus fruits and juices. Results of sensory analysis indicated a bitter taste threshold of 6 ppm for limonin, and 6 ppm or 3 ppm for nomilin. Nevertheless, the contribution of nomilin to the bitter taste of juices is minor; it occurs mainly in grapefruit juice.
1.3 Chemical Solubility and Handling
Nomilin can remain in solution in ethanol containing methylene chloride and dissolves in hot 2-propanol; therefore, it is easily separated from limonin. In addition, nomilin has a tendency to form solvates with many solvents, which causes the appearance of crystals from diverse solvents to be significantly different.
2. Traditional and Historical Use
Limonoids as a class were first reported in 1864 as constituents of citrus plants from the Rutaceae family. Nomilin itself, as a specifically identified compound, belongs to the modern era of phytochemical isolation; however, the parent plants from which it is derived have documented histories of traditional medicinal application spanning centuries.
Nomilin is found in traditional Chinese medicines derived from citrus fruits, such as tangerine seed (juhe), tangerine peel (chenpi), and fructus aurantii immaturus (zhishi). These preparations have been used in Chinese medicine for purposes including digestive regulation, relief of abdominal discomfort, and the treatment of inflammatory conditions. The relevance of nomilin to such traditional preparations was recognized only after isolation techniques allowed its identification as a discrete compound.
The wide clinical uses of traditional Chinese medicine Cortex Dictamni have inspired researchers to investigate its pharmacological properties. Several studies showed that extracts or active compounds of Dictamnus species exhibited a wide range of pharmacological activities such as anti-cancer, anti-inflammatory, antimicrobial, anti-platelet-aggregation, vascular-relaxing, anti-insect, anti-HIV, anti-allergic, immunosuppressing, neuroprotective, mutagenic and antimutagenic, antifertility, and anti-oxidant activities. Dictamnus species are rich in limonoids; obacunone, limonin, nomilin, and their glucosides — some of the aglycones — have been shown to inhibit chemically induced carcinogenesis and a series of human cancer cell lines, with remarkable cytotoxicity against lung, colon, oral, and skin cancers in animal test systems and human breast cancer cells.
Citrus fruits more broadly have a long cross-cultural history of use in Ayurvedic, Chinese, and Mediterranean folk traditions, applied in preparations for fever, infections, and digestive ailments. While nomilin as a defined molecule could not have been intentionally employed in these traditions, it is now understood to be one of the bioactive constituents underlying some of the observed properties of citrus-derived preparations.
3. Key Constituents, Structure, and Related Compounds
Nomilin belongs to a broader class of related compounds including deacetylnomilin, isolimonic acid, obacunone, obacunoic acid, isoobacunoic acid, and ichangin. Analogues of nomilin such as nomilinic acid glucoside, deacetyl nomilinic acid glucoside, deacetyl nomilin, defuran nomilin, obacunone 17β-d-glucopyranoside, nomilinic acid 17β-d-glucopyranoside, and deacetylnomilinic acid 17β-d-glucopyranoside have also been identified and shown to exhibit cytotoxicity and apoptosis-induction effects on a variety of human cancer cell lines.
Unlike bile acids, nomilin does not exhibit farnesoid X receptor (FXR) ligand activity. Although the nomilin derivative obacunone is capable of activating TGR5, limonin — the most abundant limonoid in citrus seeds — was not a TGR5 activator. This selectivity profile distinguishes nomilin and obacunone from the other major citrus limonoid.
Nomilinate was found to be the major acidic limonoid present in seedlings of Citrus limon. [14C]Nomilin was converted to at least six acidic metabolites in C. limon, one of which was identified as nomilinate. The metabolism via nomilinate represents the fifth metabolic pathway of nomilin shown to be present in nature.
4. Mechanisms of Action
4.1 Phase II Enzyme Induction (Chemopreventive Mechanism)
Nomilin enhances the elimination of toxic electrophiles by phase II detoxifying enzymes such as glutathione-S-transferase (GST). Nomilin was shown to be a potent inducer of phase II drug metabolism and detoxifying enzymes' GST activity in the liver, the small intestinal mucosa, and the forestomach, but not in the lung and colon, in mice.
Limonin and nomilin, two of the most abundant limonoids, have been found to inhibit chemically induced carcinogenesis. Both compounds are inducers of glutathione S-transferase, a major detoxifying enzyme system. The increased enzyme activity was correlated with the ability of these compounds to inhibit carcinogenesis.
4.2 Anti-inflammatory Signaling: NF-κB Pathway
Nomilin induces apoptosis through both extrinsic and intrinsic pathways in TNF-α-induced human aortic smooth muscle cells (HASMCs) and inhibits smooth muscle cell proliferation. Nomilin also suppresses the phosphorylation of IκB, reduces nuclear localization of activated NF-κB, and decreases downstream inflammatory signaling.
In IL-1β-stimulated chondrocytes, nomilin pre-treatment suppressed the over-regulation of pro-inflammatory factors such as NO, IL-6, PGE2, iNOS, TNF-α, and COX-2. Nomilin also down-regulates the degradation of extracellular matrix induced by IL-1β. Mechanistically, nomilin suppresses NF-κB signalling via disassociation of Keap1-Nrf2 in chondrocytes.
4.3 TGR5 Receptor Agonism (Metabolic Mechanism)
Nomilin was demonstrated to be an activator of TGR5. TGR5 (also known as G protein-coupled bile acid receptor 1, GPBAR1) is a G protein-coupled bile acid receptor that is expressed in many diverse tissues. TGR5 is thought to be a promising drug target for metabolic diseases because activation of TGR5 prevents obesity and hyperglycemia in mice fed a high-fat diet. Using TGR5 reporter assays, nomilin was confirmed as a TGR5 agonist, showing direct activation comparable to known agonists. These metabolic benefits were associated with increased cAMP signaling, a downstream effector of TGR5.
Human TGR5 shows higher nomilin responsiveness than does mouse TGR5, despite their high homology. Several mouse-human TGR5 chimeras were developed to ascertain the critical region for nomilin response.
4.4 Anti-cancer: Apoptosis, PI3K/Akt, and Anti-metastatic Pathways
Through protein-protein interaction (PPI) network analysis, eight core targets of nomilin against triple-negative breast cancer (TNBC) were pinpointed, namely BCL2, Caspase3, CyclinD1, EGFR, HSP90AA1, KRAS, PARP1, and TNF. Molecular docking, molecular dynamics simulation, and proteome microarray revealed that nomilin exhibits strong binding activity to these core proteins. Enrichment analysis indicated that the anti-TNBC effect of nomilin is associated with the PI3K/Akt pathway. In vitro and in vivo experiments demonstrated that nomilin inhibits TNBC cell proliferation and migration while promoting cell apoptosis through the PI3K/Akt pathway.
Treatment with nomilin induced an apoptotic response characterized by an increase in the sub-G1 fraction of cells with chromatin condensation and membrane blebbing, a typical ladder of DNA fragmentation, and detection of apoptotic cells by TUNEL assay.
4.5 Antiviral Mechanism
Nomilin was effective in inhibiting HIV-1 replication in all cellular systems tested, including in vitro infected human peripheral blood mononuclear cells (PBMC), naturally infected PBMC, and in vitro infected monocyte-derived macrophages. The mechanism of the antiviral action of nomilin is considered to suppress in vitro HIV-1 protease activity.
4.6 Osteoclastogenesis: RANKL-MAPK Pathway Suppression
Treatment with nomilin significantly inhibited the formation of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated osteoclasts from both RAW 264.7 cells and bone marrow-derived macrophages. Nomilin also decreased bone-resorption activity and pit formation area of osteoclasts. Furthermore, nomilin could downregulate the expression levels of osteoclast genes NFATc1 and TRAP, and suppress RANKL-induced MAPK signaling pathways.
4.7 Neuroprotection: Nrf2/NQO1 Pathway
NOM treatment significantly mitigated cell death and decreased lactate dehydrogenase (LDH) release and ROS production in SH-SY5Y cells induced by oxygen-glucose deprivation (OGD), an effect almost abolished by Nrf2 knockdown. NOM also improved infarct area, brain edema, and neurological deficits in an experimental stroke rat model via middle cerebral artery occlusion (MCAO).
4.8 Neuropsychiatric: GABAergic Circuit Modulation
Nomilin ameliorates LPS-induced depressive-like behaviors in mice by activating LSv GABAergic neurons and the LSvGABA → BNST neural circuit, with downstream modulation mediated by GABAA receptors.
5. Scientific Evidence by Area of Activity
5.1 Anticancer Activity
Strong and compelling evidence from preclinical research suggests that nomilin has the capacity to inhibit the growth and proliferation of many types of cancers, act as an anti-inflammatory agent, and modulate the severity of human immunodeficiency virus infections.
In vitro evidence: Nomilin possesses antiproliferative activity against a number of human cancer cell lines, including those for leukemia (HL-60) and cancers of the ovary (SKOV-3), cervix (HeLa), stomach (NCI-SNU-1), liver (Hep G2), and breast (MCF-7).
In vivo (animal) evidence — metastasis: Nomilin is a triterpenoid present in common edible citrus fruits with putative anticancer properties. In one study, the antimetastatic potential of nomilin and its possible mechanism of action were investigated. Metastasis was induced in C57BL/6 mice through the lateral tail vein using highly metastatic B16F-10 melanoma cells. Administration of nomilin inhibited tumor nodule formation in the lungs by 68% and markedly increased the survival rate of metastatic tumor-bearing animals. Nomilin also showed an inhibition of tumor cell invasion and activation of matrix metalloproteinases.
In vivo (animal) evidence — forestomach cancer: Nomilin was found to reduce the incidence and number of tumors per mouse of forestomach tumors induced by benzo[a]pyrene. Topical application of the limonoids was found to inhibit both the initiation and the promotion phases of carcinogenesis in the skin of SENCAR mice.
Triple-negative breast cancer (TNBC), in vitro and in vivo: Enrichment analysis indicated that the anti-TNBC effect of nomilin is associated with the PI3K/Akt pathway. In vitro and in vivo experiments demonstrated that nomilin inhibits TNBC cell proliferation and migration while promoting cell apoptosis through the PI3K/Akt pathway.
Phase II enzyme induction (animal study): The purpose of one study was to evaluate how variations in the structures of citrus limonoids — namely nomilin, deacetyl nomilin, and isoobacunoic acid — would influence phase II enzyme activity in excised tissues from a mouse model. Female A/J mice were treated with three limonoids and a mixture to evaluate their effect on phase II enzymes in four different tissues. Assays for glutathione S-transferase (GST) and NAD(P)H:quinone reductase (QR) were used to evaluate induction of phase II enzymatic activity. Nomilin significantly induced GST activity against 4-nitroquinoline 1-oxide (4NQO) in the intestine (280%) and stomach (75%).
Evidence strength: The anticancer evidence for nomilin is currently restricted to in vitro cell-line studies and in vivo animal models. No clinical trials in humans have been published investigating nomilin as an anticancer intervention. The findings are preliminary and hypothesis-generating.
5.2 Anti-obesity and Metabolic Effects
Animal study (key mechanistic study): In one study, nomilin was identified as a naturally occurring activator of TGR5. Unlike bile acids, nomilin did not exhibit farnesoid X receptor ligand activity. Although the nomilin derivative obacunone was capable of activating TGR5, limonin was not a TGR5 activator. When male C57BL/6J mice fed a high-fat diet (HFD) for 9 weeks were further fed a HFD either alone or supplemented with 0.2% w/w nomilin for 77 days, nomilin-treated mice had lower body weight, serum glucose, serum insulin, and enhanced glucose tolerance.
A wide range of bioactive natural compounds including nomilin are examined for their ability to modulate TGR5 signaling and elicit favorable metabolic effects. These metabolic benefits were associated with increased cAMP signaling, a downstream effector of TGR5.
Evidence strength: The anti-obesity and anti-hyperglycemic data for nomilin are derived entirely from animal models, predominantly high-fat diet mouse studies. The dosage used in the key study was 0.2% w/w nomilin added to the diet for 77 days. No human clinical trials have been conducted to validate these findings. The specificity of TGR5 agonism provides a plausible mechanism, and the notably higher responsiveness of human TGR5 to nomilin compared to mouse TGR5 is a potentially favorable translational indicator, but this has not yet been tested clinically.
5.3 Anti-inflammatory and Cardiovascular Effects
In vitro (smooth muscle cell study): Treatment with nomilin could significantly inhibit TNF-α-induced proliferation in human aortic smooth muscle cells (HASMCs). Additionally, nomilin markedly reduced the phosphorylation levels of the inhibitor of NF-κB (IκBα) and suppressed the inflammatory reaction in TNF-α-treated HASMCs. These results indicated that the anti-proliferative activity of nomilin on TNF-α-induced HASMCs results from apoptosis through inhibition of NF-κB-mediated inflammatory signaling, which may be beneficial in the context of atherosclerosis.
Osteoarthritis (in vitro and in vivo): A study demonstrated the latent mechanism of nomilin in alleviating the progress of osteoarthritis (OA) in both in vitro and in vivo studies. The results showed that nomilin pre-treatment suppressed the IL-1β-induced over-regulation of pro-inflammatory factors such as NO, IL-6, PGE2, iNOS, TNF-α, and COX-2. Nomilin also down-regulated the degradation of extracellular matrix induced by IL-1β. Mechanistically, nomilin suppressed NF-κB signaling via disassociation of Keap1-Nrf2 in chondrocytes. Furthermore, nomilin delays disease progression in the mouse OA model.
Evidence strength: Anti-inflammatory evidence is confined to in vitro cell studies and animal models. No randomized controlled trials in human subjects have been published.
5.4 Antiviral Activity
HIV-1 (in vitro): Nomilin was reported to be effective in inhibiting HIV-1 replication in all cellular systems used, including in vitro infected human peripheral blood mononuclear cells (PBMC), naturally infected PBMC, and in vitro infected monocyte-derived macrophages, which is one of the most important viral reservoirs in vivo. The mechanism of the antiviral action of nomilin is considered to suppress HIV-1 protease activity in vitro.
Recently, nomilin was also reported to inhibit SARS-CoV-2 virucidal activity effectively in Vero E6 cells.
Evidence strength: The antiviral data for nomilin are from in vitro laboratory studies only. There are no human clinical trials on nomilin for any viral infection.
5.5 Osteoclastogenesis and Bone Health
In vitro evidence: Nomilin significantly reduced the number of TRAP-positive multinucleated cells, bone resorption activity, the expression of some osteoclast genes, and the levels of NFATc1 and TRAP mRNA, and inhibited the phosphorylation of ERK, p38, and JNK in the MAPK signaling pathways. These results suggested that nomilin could inhibit the phosphorylation of MAPKs induced by RANKL and significantly suppress the differentiation of osteoclasts in vitro, demonstrating potential application for prevention of bone metabolic diseases.
Evidence strength: This evidence is limited to in vitro cell culture. No animal model data or clinical trials for bone health endpoints in humans have been published for nomilin.
5.6 Neuroprotection
In vitro and in vivo (ischemia-reperfusion model): Oxidative stress plays an important role in cerebral ischemia-reperfusion injury. The Nrf2/NQO1 pathway has been considered as a potential target for neuroprotection. Nomilin is a limonoid compound obtained from extracts of citrus fruits. The study determined whether nomilin could exert beneficial effects in cerebral ischemia-reperfusion rats. Nomilin treatment significantly mitigated cell death and decreased LDH release and ROS production in SH-SY5Y cells induced by oxygen-glucose deprivation (OGD), an effect almost abolished by Nrf2 knockdown. Nomilin also improved infarct area, brain edema, and neurological deficits in an experimental stroke rat model via middle cerebral artery occlusion (MCAO).
Evidence strength: Neuroprotective evidence is restricted to in vitro and animal models of ischemia. No human clinical data exist.
5.7 Antidepressant Effects
Animal study (2025): In a study using lipopolysaccharide (LPS)-induced and chronic restraint stress (CRS)-induced depression mouse models, the antidepressant effects of nomilin were verified. Brain regions with altered activity after nomilin administration were identified using c-fos immunofluorescence staining. Chemogenetics, viral tracing, fiber photometry, and pharmacological strategies were conducted to further investigate the neural circuit mechanisms of nomilin's antidepressant effects. Activation of LSv GABAergic neurons alleviated LPS-induced depressive-like behaviors, whereas their inhibition attenuated the antidepressant effects of nomilin. These findings underscore the critical role of LSv GABAergic neurons in mediating the antidepressant effects of nomilin.
Evidence strength: This is a 2025 preclinical mouse study. No human data on nomilin as an antidepressant exists.
5.8 Immunomodulatory Effects
In vivo, nomilin increases white blood cell counts and antibody titers but suppresses delayed-type hypersensitivity reactions. Nomilin was found to enhance the total white blood cell count, bone marrow cellularity, α-esterase-positive cells, antibody titer, and the number of plaque-forming cells in the spleen, while also remarkably inhibiting delayed-type hypersensitivity reaction in Balb/c mice.
Evidence strength: Immunomodulatory data are from animal studies. No human clinical immunomodulation trials have been conducted for nomilin.
5.9 Antioxidant Activity
The antioxidant capacities of limonin and nomilin vary in different tissues and cultivars. In three tissue types other than albedo, the antioxidant capacities of limonin and nomilin were high — 2.9 to 8.3 times that of vitamin C.
Studies have demonstrated that nomilin shows anticancer, anti-inflammatory, antioxidant, anti-obesity, and blood glucose-regulating properties. Specific mechanisms include inhibition of cancer cell proliferation through modulation of cell signaling pathways, suppression of inflammatory responses, delay of aging through radical scavenging, and improvement of metabolic syndrome via modulation of metabolic pathways.
6. Body Systems and Health Areas of Association
- Oncology / Cancer Biology: Antiproliferative, pro-apoptotic, and antimetastatic effects demonstrated in multiple cancer cell lines and animal tumor models (leukemia, ovary, cervix, stomach, liver, breast, melanoma, TNBC).
- Metabolic / Endocrine System: TGR5 agonism linked to anti-obesity and anti-hyperglycemic effects in high-fat diet animal models.
- Cardiovascular System: Inhibition of smooth muscle cell proliferation and NF-κB-mediated inflammation relevant to atherogenesis.
- Musculoskeletal System: Suppression of osteoclastogenesis via RANKL-MAPK pathway and amelioration of osteoarthritis in animal models.
- Nervous System: Protection against ischemia-reperfusion injury via Nrf2/NQO1; antidepressant effects via LSv GABAergic neurons in animal models.
- Immune System: Immunomodulatory effects including enhancement of antibody responses and modulation of delayed-type hypersensitivity.
- Virology: In vitro inhibition of HIV-1 protease and SARS-CoV-2 virucidal activity.
- Gastrointestinal / Detoxification: Induction of hepatic and intestinal phase II enzymes (GST, QR), relevant to carcinogen detoxification.
7. Dosage Forms and Dosages Reported in Studies
Nomilin is not currently approved as a pharmaceutical drug in any jurisdiction and has no established human clinical dosage. The following dosages are those reported in preclinical research contexts and should be understood as experimental parameters only:
- High-fat diet obesity model (mice): Male C57BL/6J mice fed a HFD were further fed a HFD either alone or supplemented with 0.2% w/w nomilin for 77 days, resulting in lower body weight, serum glucose, serum insulin, and enhanced glucose tolerance.
- Phase II enzyme induction (mice): In an in vivo study using female A/J mice, nomilin (derived from Citrus × aurantium L. sour orange seed powder) induced GST at a dose of 20 mg administered by oral gavage once every two days, for four administrations.
- Antimetastatic study (mice): Metastasis was induced in C57BL/6 mice via B16F-10 melanoma cells, and administration of nomilin inhibited tumor nodule formation in the lungs by 68%. Specific doses were not reported in the available abstract data.
A number of studies have demonstrated that nomilin and its analogues exhibit a variety of biological and pharmacological activities. These include anti-cancer, immune-modulatory, anti-inflammatory, anti-obesity, anti-viral, anti-osteoclastogenic, anti-oxidant, and neuro-protective effects. However, the translation of any specific effective dose to human application remains speculative pending clinical trials.
8. Safety Considerations
Formal human safety and toxicology data for nomilin as an isolated compound are not available in the published scientific literature. The following safety-relevant observations are drawn from preclinical or indirect sources:
8.1 Dietary Context and GRAS Status
Nomilin is a naturally occurring constituent of commonly consumed citrus fruits, including oranges, lemons, grapefruits, and mandarins, where it occurs at low concentrations as both an aglycone and glucoside. Limonoids can be present as water-soluble "tasteless" glucosides and as water-insoluble "bitter" aglycones; both limonin and nomilin are responsible for the bitterness of citrus fruits and juices. Human dietary exposure through normal fruit and juice consumption is therefore established and long-standing.
8.2 Bitterness and Organoleptic Properties
Results of sensory analysis indicated a bitter taste threshold of 6 ppm for limonin, and 6 ppm or 3 ppm for nomilin. The contribution of nomilin to the bitter taste of juices is minor; it occurs mainly in grapefruit juice. At higher concentrations such as those that might be used in an isolate supplement form, bitter taste may be a practical consideration.
8.3 Selectivity at TGR5 vs. FXR
Nomilin was identified as an activator of TGR5. Unlike bile acids, nomilin did not exhibit farnesoid X receptor (FXR) ligand activity. This selectivity is considered potentially favorable because FXR activation is associated with distinct metabolic effects including alterations in bile acid synthesis and lipid metabolism. The absence of FXR activity suggests nomilin may act more specifically through TGR5 without triggering FXR-related pathways.
8.4 TGR5 and Gallbladder Considerations
Emerging strategies in TGR5-directed drug development include gut-restricted agonism to minimize gallbladder-related side effects. TGR5 is expressed in the gallbladder, and systemic TGR5 agonism has been associated with gallbladder filling in preclinical models for some TGR5 agonists. Whether nomilin at any dose relevant to supplementation produces this effect has not been established in published human data.
8.5 Differential Species Responsiveness
The agonist effect of nomilin on mouse TGR5 was much weaker than on human TGR5, as demonstrated by cAMP response element-luciferase reporting analysis in HEK293 cells. This interspecies difference means that the dosages active in mouse models may not be directly predictive of those needed or safe in humans.
8.6 Absence of Human Clinical Trial Data
No published randomized controlled trials, pharmacokinetic studies, or formal safety evaluations of isolated nomilin as a dietary supplement or pharmaceutical have been identified in peer-reviewed literature. All pharmacological dose-response data originate from cell culture and animal experiments. Nomilin and its analogues have emerged as a potential therapy for human diseases, and the purpose of recent reviews is to chronicle the evolution of nomilin research from examining its history, structure, and occurrence to its pharmacological and disease-preventing properties, as well as its potential utilization in medicine and food science. The current research landscape is therefore exploratory and pre-clinical.
8.7 Extraction Solvents and Preparation Methods
The method of extraction with supercritical fluids has advantages over traditional extraction with liquid organic solvents due to its environmental compatibility. Supercritical fluids have several other advantages, such as nontoxicity, nonflammability, inability to leave residual chemicals, and low to moderate operating temperatures and pressures. The method of extraction used to prepare nomilin for research or commercial purposes may influence the purity of the compound and the presence of co-extracted materials.
References
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