Sinigrin

Sinigrin: A Comprehensive Reference Article

1. Identity and Chemical Characterization

Names and Classification

Sinigrin (allyl-glucosinolate or 2-propenyl-glucosinolate) is a natural aliphatic glucosinolate present in plants of the Brassicaceae family, such as broccoli and Brussels sprouts, and the seeds of Brassica nigra (mustard seeds), which contain high amounts of sinigrin. Its molecular formula is C₁₀H₁₇NO₉S₂ (PubChem CID 6911854). In its naturally occurring potassium salt form, sinigrin carries the molecular formula C₁₀H₁₆KNO₉S₂ and the CAS Registry Number 3952-98-5. Its chemical structure comprises three distinct components: a sulfonated aldehyde oxime group, a β-D-thioglucose moiety, and an amino acid-derived allyl group.

The chemical structure confirmed it is a glucose derivative with β-D-glucopyranose configuration. It was unclear whether the C=N bond was in the Z (or syn) form, with sulfur and oxygen substituents on the same side of the double bond, or the alternative E form. The matter was settled by X-ray crystallography of its potassium salt in 1963. It is now known that all natural glucosinolates are of Z form.

This unique molecular configuration endows sinigrin with remarkable chemical stability and a spectrum of specific biological activities within living organisms.

Discovery and Structural Elucidation

The compound was first reported in 1839, after its isolation from black mustard Brassica nigra, after which it was named. The chemical structure of sinigrin had been established by 1930. The first laboratory synthesis of sinigrin was published in 1965.

Biosynthesis

Sinigrin is biosynthesized from the amino acid methionine in a multi-step pathway. Sinigrin is unusual among the glucosinolates because it is also known to be the natural precursor for other volatile compounds including epithionitrile, allyl cyanide, and allyl thiocyanate.

2. Natural Sources and Botanical Distribution

Sinigrin is a glucosinolate that belongs to the family of glucosides found in some plants of the family Brassicaceae such as Brussels sprouts, broccoli, and the seeds of black mustard (Brassica nigra). Sinigrin is now known to occur widely in other brassica families including Brassicaceae and Capparaceae.

It is a major glucosinolate associated with the family of glucosides present in the Brassicaceae family, such as the seeds of black mustard (Brassica nigra), Brussels sprouts, and broccoli. It has been reported that Brassica juncea (Indian mustard) contains significant amounts of sinigrin. Sinigrin is a natural compound found in the seeds of Brassica plants including many traditional Chinese medicines such as Descurainiae Semen, Raphani Semen, and Sinapis Semen.

B. nigra contains an isothiocyanate glycoside named sinigrin and myrosin, which yield 0.7–1.3% mustard volatile oil. Over 90% of this oil is allyl isothiocyanate.

Seeds of white mustard, Sinapis alba, give a less pungent mustard because this species contains a different glucosinolate, sinalbin.

Role in Plant Defense

The natural role of glucosinolates is as plant defense compounds. The enzyme myrosinase removes the glucose group in sinigrin to give an intermediate which spontaneously rearranges to allyl isothiocyanate, the compound responsible for the pungent taste of Dijon mustard. This is a reactive material which is toxic to many insect predators, and its production is triggered when the plant is damaged. This effect has been called the "mustard oil bomb."

3. Traditional and Historical Use

Ancient Civilizations and Classical Antiquity

The use of the mustard plant for medicinal purposes goes back several millennia. Mustard was used as both a condiment and medicine by the ancient Egyptians, Sumerians, and Chinese. Historically, mustard plasters trace their origins to ancient civilizations, including Egypt, China, and Rome, where mustard seeds were valued for both culinary and medicinal purposes as early as 2000 BCE.

The first century CE Greek physician Dioscorides prescribed mustard for everything from tonsillitis to epilepsy, and the Romans combined ground mustard seed with vinegar to make an ointment for snakebites and scorpion stings and chewed the seed to relieve toothaches. The most common medicinal use of mustard through the centuries was the mustard plaster, first recommended by Hippocrates as a treatment for pulmonary illnesses and rheumatism.

Dioscorides believed in the use of mustard in plasters and poultices as an important part of treatment not only for aches and congestions, but also for easing the pain and discomfort of pregnancy and childbirth. The heat generated by the poultice created a soothing warmth and relaxation of muscles — but only if it was not left on the body for too long. Because of that heat, mustard could also cause skin burns if not carefully attended.

The use of Khardal (Brassica nigra) has been in practice from prehistoric times in the form of mustard plaster, which was first described by Dioscorides (circa 1st century CE).

Mustard Plaster Preparation

Although there are various recipes for making a plaster, all basically use ground mustard seed, preferably from the pungent black variety, and flour mixed with water. The paste is then wrapped in a flannel or other cloth and placed on the affected area, the original theory being that the heat caused by the substances in the mustard would promote circulation. Allyl isothiocyanate is not present in significant amounts in dry mustard seed powder but is generated in situ when the powder is mixed with water to form the plaster. This occurs through the enzymatic hydrolysis of sinigrin, the predominant glucosinolate in black and brown mustard seeds (Brassica nigra and Brassica juncea), catalyzed by the enzyme myrosinase, which is released upon seed disruption or hydration.

This application aims to stimulate blood flow, reduce inflammation, and alleviate symptoms such as chest congestion, muscle aches, and joint pain by drawing heat and circulation to the affected area.

Spread Through Europe and Beyond

By the late 1500s, the use of mustard plasters had spread to England and other parts of Europe, and then to the New World. In the late 1700s and early 1800s, doctors in Russia were using them as a treatment for mental illness and Spanish missionaries in California for a variety of illnesses. By the 19th and early 20th centuries, they became a staple in Western conventional medicine, often prescribed for respiratory ailments like bronchitis and pneumonia, as well as rheumatic conditions.

Ayurvedic and Indian Traditional Medicine

Since ancient times, mustard has been used by mankind for its culinary as well as medicinal properties. It has been systematically described and evaluated in the classical Ayurvedic texts. Since ancient times, mustard has been used as a food and illustrated medicinal benefits in Ayurveda. The Ayurvedic tradition established mustard as a valuable herb which has therapeutic effects. For thousands of years, Indian mustard seeds and their oil have been used to relieve joint pain, fever, alleviate cough and colds, lessen swelling, and in cleaning the cranial cavity. Mustard oil has also been used for the treatment of various skin diseases and wounds.

Traditional Chinese Medicine

Sinigrin is found in seeds of Brassica plants including many traditional Chinese medicines such as Descurainiae Semen, Raphani Semen, and Sinapis Semen. It is usually used for the treatment of multiple disorders in combination with other herbs.

Mustard Seed Footbaths

Similar effects have been found in the mustard plant, which contains glucosinolates, especially sinigrin. Different studies have shown its beneficial pharmacological effects against cancer, antibacterial, antifungal, antioxidant, anti-inflammatory and wound-healing properties, and biofumigation. Mustard seed footbaths, in which sinigrin-containing seeds are combined with warm water to release allyl isothiocyanate transdermally, represent a traditional folk remedy for respiratory tract infections that persists into contemporary use in parts of Europe.

4. Key Constituents, Hydrolysis Products, and Mechanisms of Action

The Myrosinase–Sinigrin System

Cutting and chewing of cruciferous vegetables releases the thioglucosidase enzyme myrosinase, which degrades glucosinolates to isothiocyanates and other minor metabolites. Cooking of cruciferous vegetables inactivates the myrosinase enzyme, allowing intact glucosinolates to reach the large intestine, where they can be degraded by the indigenous microflora into isothiocyanates. AITC is stored stably in the plant as its precursor sinigrin (a type of glucosinolate), which is physically separated from myrosin cells containing myrosinase. Upon tissue disruption, myrosinase gets released and hydrolyzes the sinigrin to produce AITC and by-products.

Primary Hydrolysis Products

Glucosinolates are broken down enzymatically by myrosinase, mainly to isothiocyanates, cyanides, and thiocyanates, which are the main bioactives known for biological activity. The principal product of sinigrin hydrolysis is allyl isothiocyanate (AITC), which is responsible for the pungent flavor and biological activity of preparations derived from black mustard. The metabolic activation of sinigrin results in the formation of isothiocyanates which are attributed to the anti-tumour effects.

It is believed that the metabolic activation of sinigrin leads to the formation of isothiocyanates, which are responsible for contributing to the anti-tumor effects and other biological actions.

Colonic Microbial Metabolism

Cooking of cruciferous vegetables inactivates the myrosinase enzyme, allowing intact glucosinolates to reach the large intestine, where they can be degraded by the indigenous microflora into isothiocyanates. This local release of isothiocyanates may explain the protective effect of cruciferous vegetables on the colon epithelium. In an in vitro model first set up with a pooled and cultured human microflora, 1–4% of sinigrin at various concentrations was converted into AITC. However, the conversion rate was remarkably higher if different individual human microflora were used — between 10% and 30% (mean 19%) of the sinigrin was converted into allyl isothiocyanate. Peak levels of allyl isothiocyanate were observed between 9 and 12 hours after the addition of sinigrin.

Anti-inflammatory Signaling Pathways

Sinigrin demonstrates efficacy in modulating critical signaling pathways, such as nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK), effectively suppressing the production of pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β). Its inherent antioxidant properties synergistically enhance its anti-inflammatory effects.

Antiglycation Activity

Sinigrin was found to be a potent inhibitor for both the early (Amadori product) and advanced glycation end products (AGEs). In addition, in vitro glycation studies of lens crystallin demonstrated the strong antiglycation activity of sinigrin.

5. Scientific Evidence by Area of Use

5.1 Anticancer Activity

Overview: A number of studies have been performed on the therapeutic activities of sinigrin and revealed its anticancer, anti-inflammatory, antibacterial, antifungal, antioxidant, and wound healing effects. The overwhelming majority of this work is preclinical (cell-based and animal studies); no clinical human trials evaluating sinigrin specifically as an anticancer intervention have been published.

Cell Line Studies: An MTT assay was performed for a sinigrin-rich fraction using three different human cancer cell lines: prostate cancer (DU-145), colon adenocarcinoma (HCT-15), and melanoma (A-375). Cell-based assays were extended to conduct apoptotic and caspase-3 activities, to determine the mechanism of action of sinigrin. MTT assay showed IC₅₀ values of 15.88, 21.42, and 24.58 µg/mL for DU-145, HCT-15, and A-375 cell lines, respectively. Increased cellular apoptosis and caspase-3 expression were observed with the sinigrin-rich fraction, indicating significant overexpression of caspase-3 in DU-145 cells.

Bladder Cancer (Preclinical): Mustard seed powder (MSP-1) was used to inhibit bladder cancer growth, development, and muscle invasion. MSP-1 stores AITC in its inactive form, sinigrin, which is hydrolyzed to AITC in the presence of endogenous myrosinase enzymes. During in vitro experiments, hydrated MSP-1 caused G2/M phase cell cycle arrest and apoptosis in rat bladder cancer AY-27 cells and human bladder cancer UM-UC-3 cells.

Liver Cancer (Animal Model): A study examined the efficacy of sinigrin on liver cancer caused by diethylnitrosamine (DEN) in mice, analyzing its impact on the Nrf-2/HO-1, PI3K–Akt–mTOR, and apoptotic pathways. Development of liver cancer was induced by intraperitoneal injection at the age of 14 days with DEN (25 mg/kg) in mice. Thereafter, sinigrin was orally administered at doses of 10 and 20 mg/kg body weight per day for the last 28 days. At the end of 10 weeks, mice were sacrificed and hepatic biochemical and molecular assessments were conducted. Sinigrin reduced the serum level of alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), alpha-fetoprotein (AFP), and bilirubin, but increased total protein and albumin levels.

Lung Cancer (Preclinical): Sinigrin has been shown to inhibit PD-L1 expression via the JAK-STAT signaling pathway and modulate the immune microenvironment of lung cancer in preclinical settings.

Additional Tumor Types: Numerous studies indicate the positive effects of sinigrin in preventing the growth and development of tumors of the tongue, esophagus, small and large intestines, breast, and urinary bladder. These findings remain primarily in vitro or in animal models.

Evidence Strength: All anticancer evidence for sinigrin itself is at the preclinical stage (cell culture and rodent models). No human clinical trials evaluating sinigrin as a standalone anticancer agent have been identified. Findings are preliminary and exploratory.

5.2 Anti-inflammatory Activity

Sinigrin, an aliphatic glucosinolate abundantly present in cruciferous vegetables, has garnered attention for its significant anti-inflammatory, antioxidant, antibacterial, and anticancer properties. Chronic inflammatory diseases — including asthma, ulcerative colitis, diabetes, and atherosclerosis — pose substantial challenges to modern medicine, necessitating novel therapeutic strategies.

Sinigrin demonstrates efficacy in modulating critical signaling pathways, such as NF-κB and MAPK, effectively suppressing the production of pro-inflammatory cytokines like TNF-α, IL-6, and IL-1β. Its inherent antioxidant properties synergistically enhance its anti-inflammatory effects.

Evidence Strength: The anti-inflammatory mechanisms have been characterized through systematic review of preclinical data (in vitro and animal studies). Direct human interventional evidence is absent; evidence is currently mechanistic and preclinical.

5.3 Antioxidant Activity

Glucosinolates have been reported to exhibit different pharmacological properties, such as antifungal, antibacterial, bioherbicidal, antioxidant, antimutagenic, anticancer, and anti-inflammatory effects. Sinigrin was found to be a potent inhibitor for both the early (Amadori product) and advanced glycation end products (AGEs). In vitro glycation studies of lens crystallin demonstrated the strong antiglycation activity of sinigrin.

Evidence Strength: Antioxidant activity is characterized in in vitro and computational (molecular docking) studies. No controlled human trials have assessed sinigrin's antioxidant activity in vivo.

5.4 Antibacterial and Antifungal Activity

Studies conducted on the pharmacological activities of sinigrin have revealed anti-cancer, antibacterial, antifungal, antioxidant, anti-inflammatory, wound healing properties, and biofumigation. The primary mechanism is understood to be via the release of allyl isothiocyanate upon hydrolysis, which has direct antimicrobial action. Even before Pasteur discovered that germs cause infection and disease, the antiseptic properties of mustard were recognized by barber-surgeons who used a mustard solution as a surgical scrub long before the development of antiseptic washes.

Evidence Strength: Antibacterial and antifungal evidence for sinigrin is predominantly in vitro. No human clinical trials have been conducted. Evidence remains at the preclinical exploratory stage.

5.5 Wound Healing

Sinigrin has been studied for its different biological activities such as anticancer, antimicrobial, and anti-inflammatory, but wound healing effects of sinigrin were less investigated. One study investigated the wound healing action of sinigrin on normal human keratinocytes cells (in vitro). Assessed both individually and as a phytosome complex on HaCaT cells, sinigrin, one of the main glucosinolates present in the Brassicaceae plant family, demonstrated wound healing potential. When combined with phytosomes, sinigrin healed wounds completely (100%) as opposed to the phytoconstituent alone, which only healed 71% of the wound.

Evidence Strength: Wound healing evidence is in vitro (cell-based). No clinical wound healing trials with sinigrin have been published.

5.6 Cardiometabolic Effects

Additional beneficial properties of sinigrin pertain to cardiometabolic disorders such as dyslipidemia, insulin resistance, hypertension, impaired glucose tolerance, and central adiposity. It has been established that the intake of glucosinolates in animal models of rodents fed with high-fat diets contributes to reductions in total serum cholesterol, LDL cholesterol, inflammatory cytokines, and the progression of atherosclerotic lesions and hypertension.

Evidence Strength: Cardiometabolic benefits attributed to sinigrin and related glucosinolates are based on animal studies. No human clinical data for sinigrin specifically has been identified.

5.7 Colitis / Intestinal Inflammation

Sinigrin can undergo hydrolysis in the presence of intestinal microflora exhibiting myrosinase-like activity, making it a compelling candidate for site-specific therapeutic applications in intestinal disorders such as ulcerative colitis (UC). The targeted delivery of sinigrin to the colon could leverage the enzymatic activity of gut microflora to release bioactive AITC in situ, offering localized anti-inflammatory effects for UC management.

A preclinical study developed starch nanoparticles to encapsulate sinigrin and improve its colonic delivery. In vivo studies using a preclinical UC mouse model demonstrated that the sinigrin-lecithin–starch nanoparticle system effectively targeted and released sinigrin into the intestine, where it was converted into the bioactive compound allyl isothiocyanate through the intestinal microflora.

Evidence Strength: Evidence is exclusively from animal/in vitro models. Human clinical trials are absent.

5.8 Respiratory Use (Traditional/Pilot Human Data)

Similar effects have been found in the mustard plant, which contains glucosinolates, especially sinigrin. Different studies have shown its beneficial pharmacological effects against cancer, antibacterial, antifungal, antioxidant, anti-inflammatory and wound-healing properties, and biofumigation. A pilot study evaluated mustard seed footbaths (containing sinigrin-rich mustard) for upper respiratory tract infections. The combination of thermogenic substances like mustard and warm footbaths could have a beneficial effect on the perception of illness. This pilot study was small and non-confirmatory; the evidence for sinigrin's specific role in respiratory conditions in humans remains preliminary and indirect.

5.9 Biofumigation

The allyl isothiocyanate produced from sinigrin is a reactive material which is toxic to many insect predators and its production is triggered when the plant is damaged. The biofumigation application of sinigrin-containing plant materials (incorporation of macerated Brassica matter into soil) exploits the hydrolytic release of AITC to suppress soil-borne pathogens and pests, and is an established agricultural application documented in the research literature.

6. Body Systems and Health Areas Associated with Sinigrin

• Oncology / Cell Biology: Anticancer activity studied across multiple cancer types; mechanisms include apoptosis induction, cell cycle arrest, and modulation of NF-κB, Nrf2/HO-1, PI3K–Akt–mTOR, and JAK-STAT pathways.
• Gastrointestinal System: Metabolism by colonic microflora; potential in inflammatory bowel disease (ulcerative colitis); cruciferous vegetables containing glucosinolates have been suggested to possess anticarcinogenic activity relevant to colorectal epithelium.
• Cardiovascular and Metabolic System: Preclinical evidence for effects on dyslipidemia, hypertension, and atherosclerosis via glucosinolate intake in high-fat diet animal models.
• Immune / Inflammatory System: Modulation of NF-κB and MAPK pathways; suppression of TNF-α, IL-6, and IL-1β; anti-inflammatory effects noted in systematic review-level preclinical literature.
• Skin / Wound Healing: In vitro evidence from keratinocyte models, with phytosome formulations shown to enhance healing in cell cultures.
• Endocrine System (Thyroid): Potential goitrogenic effects from excess intake (see Safety section).
• Respiratory System: Traditional counterirritant use (plasters, footbaths); pilot-level human evidence only.
• Musculoskeletal System: Traditional use in mustard plasters for joint and muscle pain; pharmacological basis is AITC-mediated counterirritant action.

7. Dosage Forms and Dosages Reported in Studies

No standardized or regulatory-approved dose of sinigrin as an isolated supplement has been established. The following dosages and forms appear in the peer-reviewed literature:

• Oral (animal model — liver cancer): Sinigrin was orally administered at doses of 10 and 20 mg/kg body weight per day for the last 28 days of a 10-week study in mice.
• In vitro (anticancer cell lines): MTT assay showed IC₅₀ values of 15.88, 21.42, and 24.58 µg/mL for DU-145 (prostate), HCT-15 (colon), and A-375 (melanoma) cell lines, respectively.
• In vitro (HPLC quantification range): A good linearity was achieved within the concentration range of 50 to 800 µg/mL for sinigrin quantification.
• Colonic model (in vitro): In a model inoculated with pooled and cultured human microflora, 1 and 15 mM concentrations of sinigrin were used.
• Phytosome formulation (in vitro wound healing): Sinigrin was formulated into phytosomes (bound to phospholipids, mainly phosphatidylcholine) to increase its bioavailability and enhance wound healing efficacy in cell-based assays.
• Nanoparticle delivery (preclinical colitis model): A novel delivery system was developed using starch nanoparticles to encapsulate sinigrin via a sinigrin-lecithin complex, significantly improving encapsulation efficiency, stability against acidic degradation, and controlled release in simulated intestinal conditions.

No human clinical dose-ranging or pharmacokinetic studies for sinigrin as an isolated oral supplement have been identified in the peer-reviewed literature at this time.

8. Bioavailability and Delivery Challenges

The clinical application of sinigrin faces significant challenges. Due to its small, hydrophilic nature, sinigrin is prone to rapid systemic clearance upon oral administration, resulting in poor bioavailability.

It is possible to make phytoactives or plant extracts more effective by formulation to increase bioavailability and resolve solubility issues, thus enhancing the biological profile or therapeutic potential. One strategy involves formulating sinigrin into phytosomes (also known as herbosomes) to increase bioavailability and enhance therapeutic efficacy. Phytosomes are formed by a process in which the plant extract or bioactives are bound to phospholipids, mainly phosphatidylcholine, making a lipid-compatible molecular complex. The water-soluble phytoconstituents are thereby converted into lipid-compatible molecular complexes.

At concentrations typically found in foods, the glucosinolates are not toxic to humans and can be useful flavor components.

9. Safety Considerations

General Toxicological Profile

Despite a significant portion of in vivo and in vitro studies indicating the positive effects of glucosinolates, some studies point out that the excessive consumption of cruciferous vegetables leads to an excessive intake of glucosinolates, which can then be converted into toxic products through the action of the enzyme myrosinase, subsequently leading to the development of undesirable toxic and anti-nutritional effects.

Thyroid and Goitrogenic Effects

Some toxic effects of these compounds include the following: goiter due to impaired iodine availability caused by isothiocyanates; toxic effects on liver and kidney function associated with nitriles; stunted growth in animals, along with toxic effects on the liver and thyroid gland caused by goitrin; and inhibition of thyroid function leading to atrophy and goiter associated with oxazolidin-2-thione.

In an animal study examining the effects of a single dose of glucosinolates on thyroid hormones, in the sinigrin and glucotropaeolin treated groups, T3 level was reduced, possibly due to the effect of the thiocyanate ions. However, there were no significant differences between the control and treatment groups, thus more studies are needed to determine the effect of glucosinolates on thyroid hormones.

Cardiovascular Effects of AITC (Sinigrin Hydrolysis Product)

Recent studies have indicated that allyl isothiocyanate (AITC) may cause bradycardia, atrioventricular block, or abnormal electrocardiograms. These findings are primarily from preclinical or in vitro settings and have not been confirmed in controlled human studies; however, they represent a documented safety signal warranting further evaluation.

Skin Irritation (Topical Use)

The heat generated by mustard poultices created a soothing warmth and relaxation of muscles — but only if it was not left on the body for too long. Because of that heat, mustard could also cause skin burns if not carefully attended. This is a direct consequence of the topical generation of allyl isothiocyanate from sinigrin and represents a well-documented risk of traditional mustard plaster preparations.

Bioavailability and Cooking

Cooking of cruciferous vegetables inactivates the myrosinase enzyme, allowing intact glucosinolates to reach the large intestine, where they can be degraded by the indigenous microflora into isothiocyanates. This means that the bioactive profile of sinigrin consumed from cooked versus raw Brassica foods differs substantially, with raw or lightly processed plants generating significantly more AITC at the point of ingestion.

Evidence Gaps

The information on known biological activities is very limited and, hence, further studies still need to be conducted and its molecular mechanisms also need to be explored. Sinigrin is one of the glucosinolates of which the bioactivity should be explored and its known activity enhanced through optimal delivery to the human body.

References

• Mazumder A, Dwivedi A, du Plessis J. Sinigrin and Its Therapeutic Benefits. Molecules. 2016;21(4):416. PMC6273501.
• Mazumder A, Dwivedi A, du Plessis J. Sinigrin and Its Therapeutic Benefits. PubMed PMID: 27043505.
• Krul C, et al. Metabolism of sinigrin (2-propenyl glucosinolate) by the human colonic microflora in a dynamic in vitro large-intestinal model. Carcinogenesis. 2002;23(6):1009–16.
• Wikipedia. Sinigrin. (Chemical identity, history of isolation, structure).
• Veeramani C, et al. Sinigrin, a major glucosinolate from cruciferous vegetables restrains non-enzymatic glycation of albumin. Spectrochim Acta A Mol Biomol Spectrosc. 2016;155:93–101.
• Du H, et al. Deciphering the therapeutic potential of Sinigrin: A promising anti-inflammatory agent for chronic disease management. Phytomedicine. 2025.
• Du H, et al. Deciphering the therapeutic potential of Sinigrin: A promising anti-inflammatory agent for chronic disease management. PubMed PMID: 40505485.
• Zhang H, et al. Anticancer Activity, Mechanism, and Delivery of Allyl Isothiocyanate. ACS Omega. 2022. PMC9495963.
• Kotipalli RSS, et al. Development of HPLC Method for Quantification of Sinigrin from Raphanus sativus Roots and Evaluation of Its Anticancer Potential. ACS Omega. 2020. PMC7663242.
• Fahim A, et al. Potential Therapeutic Effect of Sinigrin on Diethylnitrosamine-Induced Liver Cancer in Mice: Exploring the Involvement of Nrf-2/HO-1, PI3K–Akt–mTOR Signaling Pathways, and Apoptosis. ACS Omega. 2024.
• Sinigrin inhibits PD-L1 expression via suppressing the JAK-STAT signaling pathway to modulate the tumor immune microenvironment in lung cancer. Oral Oncology. 2026.
• Mazumder A, et al. In vitro wound healing and cytotoxic effects of sinigrin–phytosome complex. Int J Pharm. 2016.
• Starch nanoparticle platform for oral delivery of sinigrin in colitis therapy. Industrial Crops and Products. 2025.
• Guo X, et al. The Effect of the Glucosinolate Sinigrin on Alterations in Molecular Biomarkers of the Myocardium in Swiss Mice. Foods. 2025;14(2):327. PMC11765020.
• Determination of Goitrogenic Metabolites in the Serum of Male Wistar Rat Fed Structurally Different Glucosinolates. PMC4112061.
• Hübner J, et al. Use of Mustard Seed Footbaths for Respiratory Tract Infections: A Pilot Study. PMC7001671.
• Hanschen FS, et al. Bioavailability of Glucosinolates and Their Breakdown Products: Impact of Processing. Frontiers in Nutrition. 2016.
• CAS Common Chemistry. Sinigrin. CAS RN 3952-98-5.
• PubChem. Sinigrin. CID 6911854. National Institutes of Health.
• World History. Brief History of Mustard Plasters.