Common Names

  • I3C
  • Indole-3-methanol
  • 3-(Hydroxymethyl)indole
  • 3-Indolylcarbinol
  • Indolylmethanol

For Patients & Caregivers

How It Works

Indole 3-carbinol has cancer-preventive effects, but it has not been shown to treat cancer in humans.

Indole-3-carbinol, also called I3C, is a resulting compound that comes from eating vegetables such as Brussels sprouts, cabbage, cauliflower, broccoli, and kale. It is known to stimulate detoxifying enzymes in the gut and liver. Because diets high in these vegetables slow cancer growth in animals, I3C is thought to be a good candidate for cancer prevention. Laboratory studies show that I3C may have anticancer activities across a variety of tumor types, and may have added benefit with some chemotherapy drugs. However, other animal studies suggest that I3C might also promote tumor growth. Additional studies and human clinical trials are needed to determine the circumstances under which I3C might be suitable for cancer prevention.

Purported Uses
  • To prevent cancer Laboratory and animal studies suggest that indole-3-carbinol may prevent a variety of cancers, including estrogen-dependent cancers, but only one clinical trial has been performed. This small study concluded that I3C can reverse cervical intraepithelial neoplasia (CIN), a condition that can lead to cervical cancer, but these findings are too limited to draw definite conclusions. In addition, some animal studies indicate that I3C supplementation might have tumor-promoting effects. More studies including clinical trials are needed.
  • To treat viral infections Preliminary studies suggest several benefits to immune function including counteracting the activity of human papiloma virus (HPV), but no studies have been conducted in humans.
Do Not Take If
  • You are taking cytochrome P450 1A2 substrate drugs: I3C may reduce the effectiveness of these drugs.
Side Effects
  • Skin rash
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For Healthcare Professionals

Scientific Name
Indole-3-Methanol, 1H-Indole-3-methanol
Clinical Summary

Indole-3-Carbinol (I3C) is a phytochemical derived from the breakdown of glucosinolates found in cruciferous vegetables including Brussels sprouts, kale, broccoli, cabbage, and cauliflower (26). Epidemiologic studies suggest that a diet high in cruciferous vegetables is associated with a lower risk of cancer and that I3C has anticarcinogenic properties across a wide range of cancers (27).

Various in vitro and in vivo studies suggest antimicrobial (28) (29), anti-inflammatory (30) (31) (32), anti-estrogenic (33) , and antiangiogenic (21) (22) effects. Antiproliferative and anticancer effects have been demonstrated in human breast (34) (35) (36) (37), prostate (38), melanoma (39), endometrial (40) , liver (41) (42), and pancreatic cancer cells (43), as well as animal models of lung (12) (23) (44), laryngeal (45), and nasopharyngeal carcinoma (46). In addition, preliminary experiments suggest I3C may potentiate or have sensitizing effects in combination with bortezomib (25) (47), tamoxifen (48), doxorubicin (49) (50), vemurafenib (51), fludarabine (52), gemcitabine (24) (43), or acetylsalicylic acid (53), and may reverse cytotoxicity with dexamethasone (54) or cardiotoxicity with doxorubicin (50) . However, these effects have not been confirmed in humans. Studies in animal carcinogenesis models suggest that I3C may also promote tumor growth (55) (56) (57) (58) (59) (60) (61). Additional studies are needed to determine under what conditions I3C could be a suitable chemopreventive agent in humans.

Data from early phase clinical trials suggested that I3C is effective against precancerous cervical dysplasia (2) and vulvar intraepithelial neoplasia (3). In premenopausal women, a supplement containing I3C and 7-hydroxymatairesinol, a dietary ingredient, increased the urinary 2:16-hydroxyestrone ratio, a known biomarker for the reduction of breast cancer risk (4). More recently, an RCT of a diindolylmethane formulation (DIM, an active I3C metabolite) in breast cancer patients on tamoxifen suggest it encourages beneficial changes in estrogen metabolism and circulating sex hormone-binding globulin levels (67).

I3C is generally well tolerated when taken orally, but it is unclear if I3C supplementation can benefit humans due to its mixed effects in preliminary studies and its ability to induce cytochrome P450 enzymes (14) (62), which may cause interactions with several medications. In addition, a recent study to measure Brassica consumption in humans suggests that the chemopreventive effects derived from cruciferous vegetable consumption may plateau and not require eating large quantities or taking high-dose supplements (68).

Food Sources

Broccoli, Brussels sprouts, cabbage, cauliflower, collards, kale, kohlrabi, mustard greens, rapeseed, rutabaga, turnips

Purported Uses
  • Cancer prevention
  • Detoxification
  • Viral infections
Mechanism of Action

Indole-3-carbinol (I3C) is a natural indolecarbinol compound derived from the breakdown of glucobrassicin produced in cruciferous vegetables such as broccoli and Brussels sprouts (39). Some of the health-protective effects of I3C are attributed to epigenetic mechanisms such as the regulation of HDAC and HAT activities and acetylation of histones and non-histone chromatin proteins (63).

Preliminary studies suggest several benefits to immune function. I3C counteracted immune evasion mechanisms of HPV16 by antagonizing E6 repression of E-cadherin (64). It decreased pro-inflammatory cytokine production and T cell activation by acting as histone deacetylase class I (HDAC-I) inhibitors (31). Other anti-inflammatory mechanisms include regulation of TIR-domain-containing adapter-inducing interferon-β (TRIF)-dependent signaling pathways (30).

In cancer cells, I3C at higher doses (>400 μM) induced apoptosis, while lower doses (<200 μM) inihbited cell growth as well as cyclin E and CDK2 expression (27). It is among compounds that exert antiproliferative and/or proapoptotic effects through regulation of one or more microRNAs (miRNAs), short noncoding RNAs that regulate gene expression by messenger RNA (mRNA) degradation or translation repression (65).

I3C may act as a chemopreventive agent for breast cancer through its estrogen receptor (ER) modulating effect (15) or upregulation of apoptotic enzyme activities (48). It disrupted ER alpha-mediated transcription within IGF1 cascade cell signaling components (34), downregulated expression of estrogen-responsive genes pS2 and cathepsin-D, and upregulated BRAC1 (17). Other inhibitory mechanisms include suppressing epithelial-to-mesenchymal transition (EMT), blocking extracellular signal-regulated kinase (ERK)/Sp1-mediated gene transcription, reducing matrix metalloproteinase (MMP)-2 and MMP-9 activities, and decreasing aromatase expression (16) (36) (37). One randomized clinical trial suggests that the decreased risk of ER-sensitive breast and cervical cancers with I3C may be due to an increase in the 2-OH-estrone:estriol metabolite ratio (18).

In HepG2 cells, I3C induced phase II and antioxidant enzymes (41). Other hepatoprotective mechanisms include immunomodulation and inhibition of pro-inflammatory cytokines and chemokines (66). Acute hepatic inflammation was suppressed via decreased miR-31 expression and subsequent caspase-2-dependent apoptosis in T cells (32). In human lung carcinoma A549 cells, I3C significantly reduced cell proliferation and induced apoptosis and cell cycle arrest at the G0/G1 phase (12). In murine models, chemopreventive effects against lung tumors occurred via reductions in levels of proinflammatory and procarcinogenic proteins (44). In melanoma cells, I3C induced G1-phase cell-cycle arrest and apoptosis by stabilization of PTEN that express wild-type PTEN (39). In prostate cancer cells, I3C inhibits androgen-dependent pathways and appeared to block the inflammatory microenvironment (38), and caused apoptosis by inhibiting Akt activation (8).

I3C coadministration with doxorubicin potentiated cytotoxic effects compared with either agent alone in pre-B acute lymphoblastic leukemia cells (49). Chemosensitive effects were produced in gemcitabine-resistant pancreatic cancer cells via microRNA-21 downregulation (43). I3C also lowered the LD50 of gemcitabine and decreased growth of pancreatic cancer cells, possibly through reactivation of the tumor suppressor gene p16INK4a (19). I3C with genistein produced synergy of apotosis and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in endometrial cancer cells (40). It reversed dexamethasone cytotoxicity via ROS inhibition and enhanced nuclear factor erythroid 2–related factor 2 (Nrf2) expression (54).

Some animal studies suggest that I3C is both an inhibitor and promoter of carcinogenesis with strong induction of placental glutathione S-transferase foci in the liver (57), and modulatory activity that included apoptotic inhibition in colon tumors (55). In addition, I3C may promote endometrial adenocarcinoma through hepatic CYP1 induction and estrogen metabolism modulation (56).

Adverse Reactions

Skin rash (5) (15)

Herb-Drug Interactions
  • Cytochrome P450 1A2 substrates: I3C induces CYP 1A2 and can reduce serum concentrations of medications metabolized by this enzyme (14) (62).
Herb Lab Interactions

In rare cases, small increases in ALT have occurred (5) (15).

Dosage (OneMSK Only)
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  3. Naik R, Nixon S, Lopes A, et al. A randomized phase II trials of indole-3-carbinol in the treatment of vulvar intraepithelial neoplasia. Int J Gynecol Cancer 2006;16(2):786-90.
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  9. Chen DZ, et al. Indole-3-carbinol and diindolylmethane induce apoptosis of human cervical cancer cells and in murine HPV16-transgenic preneoplastic cervical epithelium. J Nutr 2001;131:3294-302.
  10. Hong C, et al. Bcl-2 family-mediated apoptotic effects of 3,3’-diindolylmethane (DIM) in human breast cancer cells. Biochem Pharmacol 2002 Mar 15;63(6):1085-97.
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  14. Yoshida M, Katashima S, Ando J, et al. Dietary indole-3-carbinol promotes endometrial adenocarcinoma development in rats initiated with N-ethyl-N’-nitro-N-nitrosoguanidine, with induction of cytochrome P450s in the liver and consequent modulation of estrogen metabolism. Carcinogenesis. 2004 Nov;25(11):2257-64.
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  19. Lyn-Cook BD, Mohammed SI, Davis C, et al. Gender differences in gemcitabine (Gemzar) efficacy in cancer cells: effect of indole-3-carbinol. Anticancer Res. 2010 Dec;30(12):4907-13.
  20. Rosen CA, et al. Preliminary results of the use of indole-3-carbinol for recurrent respiratory papillomatosis. Otolaryngol Head Neck Surg 1998;118:810-5.
  21. Jin L, et al. Indole-3-carbinol prevents cervical cancer in human papilloma virus type 16 (HPV16) transgenic mice. Cancer Res 1999;59:3991-7.
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  23. Qian X, Melkamu T, Upadhyaya P, Kassie F. Indole-3-carbinol inhibited tobacco smoke carcinogen-induced lung adenocarcinoma in A/J mice when administered during the post-initiation or progression phase of lung tumorigenesis. Cancer Lett. 2011 Dec 1;311(1):57-65.
  24. Wang H, Word BR, Lyn-Cook BD. Enhanced efficacy of gemcitabine by indole-3-carbinol in pancreatic cell lines: the role of human equilibrative nucleoside transporter 1. Anticancer Res. 2011 Oct;31(10):3171-80.
  25. Taylor-Harding B, Agadjanian H, Nassanian H, et al. Indole-3-carbinol synergistically sensitises ovarian cancer cells to bortezomib treatment. Br J Cancer. 2012 Jan 17;106(2):333-43.
  26. McNaughton SA, Marks GC. Development of a food composition database for the estimation of dietary intakes of glucosinolates, the biologically active constituents of cruciferous vegetables. Br J Nutr. Sep 2003;90(3):687-697.
  27. Chen L, Cheng PH, Rao XM, et al. Indole-3-carbinol (I3C) increases apoptosis, represses growth of cancer cells, and enhances adenovirus-mediated oncolysis. Cancer Biol Ther. Sep 2014;15(9):1256-1267.
  28. Monte J, Abreu AC, Borges A, et al. Antimicrobial Activity of Selected Phytochemicals against Escherichia coli and Staphylococcus aureus and Their Biofilms. Pathogens. 2014;3(2):473-498.
  29. Julliard W, De Wolfe TJ, Fechner JH, et al. Amelioration of Clostridium difficile Infection in Mice by Dietary Supplementation With Indole-3-carbinol. Ann Surg. Jun 8 2016.
  30. Jiang J, Kang TB, Shim do W, et al. Indole-3-carbinol inhibits LPS-induced inflammatory response by blocking TRIF-dependent signaling pathway in macrophages. Food Chem Toxicol. Jul 2013;57:256-261.
  31. Busbee PB, Nagarkatti M, Nagarkatti PS. Natural indoles, indole-3-carbinol and 3,3’-diindolymethane, inhibit T cell activation by staphylococcal enterotoxin B through epigenetic regulation involving HDAC expression. Toxicol Appl Pharmacol. Jan 1 2014;274(1):7-16.
  32. Busbee PB, Nagarkatti M, Nagarkatti PS. Natural indoles, indole-3-carbinol (I3C) and 3,3’-diindolylmethane (DIM), attenuate staphylococcal enterotoxin B-mediated liver injury by downregulating miR-31 expression and promoting caspase-2-mediated apoptosis. PLoS One. 2015;10(2):e0118506.
  33. Enriquez J, Velazquez-Cruz R, Parra-Torres A, et al. The anti-estrogenic activity of indole-3-carbinol in neonatal rat osteoblasts is associated with the estrogen receptor antagonist 2-hydroxyestradiol. J Endocrinol Invest. Jun 16 2016.
  34. Marconett CN, Singhal AK, Sundar SN, et al. Indole-3-carbinol disrupts estrogen receptor-alpha dependent expression of insulin-like growth factor-1 receptor and insulin receptor substrate-1 and proliferation of human breast cancer cells. Mol Cell Endocrinol. Nov 5 2012;363(1-2):74-84.
  35. Caruso JA, Campana R, Wei C, et al. Indole-3-carbinol and its N-alkoxy derivatives preferentially target ERalpha-positive breast cancer cells. Cell Cycle. 2014;13(16):2587-2599.
  36. Ho JN, Jun W, Choue R, et al. I3C and ICZ inhibit migration by suppressing the EMT process and FAK expression in breast cancer cells. Mol Med Rep. Feb 2013;7(2):384-388.
  37. Licznerska BE, Szaefer H, Murias M, et al. Modulation of CYP19 expression by cabbage juices and their active components: indole-3-carbinol and 3,3’-diindolylmethene in human breast epithelial cell lines. Eur J Nutr. Aug 2013;52(5):1483-1492.
  38. Kim EK, Kim YS, Milner JA, et al. Indole-3-carbinol and 3’,3’-diindolylmethane modulate androgen’s effect on C-C chemokine ligand 2 and monocyte attraction to prostate cancer cells. Cancer Prev Res (Phila). Jun 2013;6(6):519-529.
  39. Aronchik I, Kundu A, Quirit JG, et al. The antiproliferative response of indole-3-carbinol in human melanoma cells is triggered by an interaction with NEDD4-1 and disruption of wild-type PTEN degradation. Mol Cancer Res. Nov 2014;12(11):1621-1634.
  40. Parajuli B, Shin SJ, Kwon SH, et al. The synergistic apoptotic interaction of Indole-3-Carbinol and Genistein with TRAIL on endometrial cancer cells. J Korean Med Sci. Apr 2013;28(4):527-533.
  41. Krajka-Kuzniak V, Paluszczak J, Szaefer H, et al. The activation of the Nrf2/ARE pathway in HepG2 hepatoma cells by phytochemicals and subsequent modulation of phase II and antioxidant enzyme expression. J Physiol Biochem. Jun 2015;71(2):227-238.
  42. Wang X, He H, Lu Y, et al. Indole-3-carbinol inhibits tumorigenicity of hepatocellular carcinoma cells via suppression of microRNA-21 and upregulation of phosphatase and tensin homolog. Biochim Biophys Acta. Jan 2015;1853(1):244-253.
  43. Paik WH, Kim HR, Park JK, et al. Chemosensitivity induced by down-regulation of microRNA-21 in gemcitabine-resistant pancreatic cancer cells by indole-3-carbinol. Anticancer Res. Apr 2013;33(4):1473-1481.
  44. Song JM, Qian X, Molla K, et al. Combinations of indole-3-carbinol and silibinin suppress inflammation-driven mouse lung tumorigenesis by modulating critical cell cycle regulators. Carcinogenesis. Jun 2015;36(6):666-675.
  45. Wang YQ, Chen C, Chen Z, et al. Indole-3-carbinol inhibits cell proliferation and induces apoptosis in Hep-2 laryngeal cancer cells. Oncol Rep. Jul 2013;30(1):227-233.
  46. Chen Z, Tao ZZ, Chen SM, et al. Indole-3-carbinol inhibits nasopharyngeal carcinoma growth through cell cycle arrest in vivo and in vitro. PLoS One. 2013;8(12):e82288.
  47. Taylor-Harding B, Agadjanian H, Nassanian H, et al. Indole-3-carbinol synergistically sensitises ovarian cancer cells to bortezomib treatment. Br J Cancer. Jan 17 2012;106(2):333-343.
  48. Malejka-Giganti D, Parkin DR, Bennett KK, et al. Suppression of mammary gland carcinogenesis by post-initiation treatment of rats with tamoxifen or indole-3-carbinol or their combination. Eur J Cancer Prev. Apr 2007;16(2):130-141.
  49. Safa M, Tavasoli B, Manafi R, et al. Indole-3-carbinol suppresses NF-kappaB activity and stimulates the p53 pathway in pre-B acute lymphoblastic leukemia cells. Tumour Biol. May 2015;36(5):3919-3930.
  50. Adwas AA, Elkhoely AA, Kabel AM, et al. Anti-cancer and cardioprotective effects of indol-3-carbinol in doxorubicin-treated mice. J Infect Chemother. Jan 2016;22(1):36-43.
  51. Kundu A, Quirit JG, Khouri MG, et al. Inhibition of oncogenic BRAF activity by indole-3-carbinol disrupts microphthalmia-associated transcription factor expression and arrests melanoma cell proliferation. Mol Carcinog. Feb 15 2016.
  52. Perez-Chacon G, Martinez-Laperche C, Rebolleda N, et al. Indole-3-Carbinol Synergizes with and Restores Fludarabine Sensitivity in Chronic Lymphocytic Leukemia Cells Irrespective of p53 Activity and Treatment Resistances. Clin Cancer Res. Jan 1 2016;22(1):134-145.
  53. Poindexter KM, Matthew S, Aronchik I, et al. Cooperative antiproliferative signaling by aspirin and indole-3-carbinol targets microphthalmia-associated transcription factor gene expression and promoter activity in human melanoma cells. Cell Biol Toxicol. Apr 2016;32(2):103-119.
  54. Lin H, Gao X, Chen G, et al. Indole-3-carbinol as inhibitors of glucocorticoid-induced apoptosis in osteoblastic cells through blocking ROS-mediated Nrf2 pathway. Biochem Biophys Res Commun. May 1 2015;460(2):422-427.
  55. Suzui M, Inamine M, Kaneshiro T, et al. Indole-3-carbinol inhibits the growth of human colon carcinoma cells but enhances the tumor multiplicity and volume of azoxymethane-induced rat colon carcinogenesis. Int J Oncol. Nov 2005;27(5):1391-1399.
  56. Yoshida M, Katashima S, Ando J, et al. Dietary indole-3-carbinol promotes endometrial adenocarcinoma development in rats initiated with N-ethyl-N’-nitro-N-nitrosoguanidine, with induction of cytochrome P450s in the liver and consequent modulation of estrogen metabolism. Carcinogenesis. Nov 2004;25(11):2257-2264.
  57. Stoner G, Casto B, Ralston S, et al. Development of a multi-organ rat model for evaluating chemopreventive agents: efficacy of indole-3-carbinol. Carcinogenesis. Feb 2002;23(2):265-272.
  58. Oganesian A, Hendricks JD, Pereira CB, et al. Potency of dietary indole-3-carbinol as a promoter of aflatoxin B1-initiated hepatocarcinogenesis: results from a 9000 animal tumor study. Carcinogenesis. Mar 1999;20(3):453-458.
  59. Kim DJ, Han BS, Ahn B, et al. Enhancement by indole-3-carbinol of liver and thyroid gland neoplastic development in a rat medium-term multiorgan carcinogenesis model. Carcinogenesis. Feb 1997;18(2):377-381.
  60. Kim DJ, Lee KK, Han BS, et al. Biphasic modifying effect of indole-3-carbinol on diethylnitrosamine-induced preneoplastic glutathione S-transferase placental form-positive liver cell foci in Sprague-Dawley rats. Jpn J Cancer Res. Jun 1994;85(6):578-583.
  61. Pence BC, Buddingh F, Yang SP. Multiple dietary factors in the enhancement of dimethylhydrazine carcinogenesis: main effect of indole-3-carbinol. J Natl Cancer Inst. Jul 1986;77(1):269-276.
  62. Tutelyan VA, Trusov NV, Guseva GV, et al. Indole-3-carbinol induction of CYP1A1, CYP1A2, and CYP3A1 activity and gene expression in rat liver under conditions of different fat content in the diet. Bull Exp Biol Med. Dec 2012;154(2):250-254.
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  64. D’Costa ZJ, Leong CM, Shields J, et al. Screening of drugs to counteract human papillomavirus 16 E6 repression of E-cadherin expression. Invest New Drugs. Dec 2012;30(6):2236-2251.
  65. Phuah NH, Nagoor NH. Regulation of microRNAs by natural agents: new strategies in cancer therapies. 2014;2014:804510.
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  67. Thomson CA, Chow HHS, Wertheim BC, et al. A randomized, placebo-controlled trial of diindolylmethane for breast cancer biomarker modulation in patients taking tamoxifen. Breast Cancer Res Treat. Aug 2017;165(1):97-107.
  68. Fujioka N, Ransom BW, Carmella SG, et al. Harnessing the Power of Cruciferous Vegetables: Developing a Biomarker for Brassica Vegetable Consumption Using Urinary 3,3’-Diindolylmethane. Cancer Prev Res (Phila). Oct 2016;9(10):788-793.
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