Crohn’s disease is an autoimmune intestinal disease of unknown etiology. The main symptoms are recurrent episodes of abdominal pain and diarrhea with weight loss, in addition to extraintestinal manifestations, including anal fistula, erythema nodosum, arthralgia, and iridocyclitis. The therapeutic drugs include 5-aminosalicylic acid preparations such as salazosulfapyridine and mesalazine; purines such as 6-mercaptopurine and azathioprine; immunosuppressive agents, mainly glucocorticoids and raglan polysaccharide tablets; and biological agents such as classical grams. The application of total enteral nutrition has also relieved the disease and alleviated pain for numerous patients. In recent years, with extensive research, there has been further understanding of the factors associated with the pathogenesis and progression of Crohn’s disease, which has catalyzed the birth and development of several novel biologic agents and therapies. Below we will provide a general overview of the drugs that may play an important role in the future treatment of Crohn’s disease: (i) Anti-adhesion molecule drugs Natalizumab (natalizumab) is a human monoclonal antibody against the α4 integrin adhesion molecule (involved in endothelial leukocyte migration), first approved by the US Food and Drug Administration (FDA) for the treatment of multiple sclerosis. Several studies have since found that natalizumab has significant efficacy in inducing and maintaining remission in Crohn’s disease. However, its off-target effects may induce progressive multifocal leukoencephalopathy. Vedolizumab, a drug that selectively acts on α4β7 integrin and the intestinal mucosal adhesion molecule MadCAM-1, has also shown promising efficacy in the treatment of Crohn’s disease. The results of the study were published in the August 2013 issue of the New England Journal. In the first part of the study, 368 patients with Crohn’s disease were randomized to two groups, treated with Vedolizumab and placebo, and evaluated for disease activity score (CDAI) at week 6. The rate of disease remission was significantly higher in patients treated with Vedolizumab than in the placebo group (14.5% versus 6.8%); the second part of patients received unblinded Vedolizumab treatment. A total of 461 patients in both parts responded to Vedolizumab treatment and were further randomized into three groups that received Vedolizumab (once every 4 weeks), Vedolizumab (once every 8 weeks) and placebo for up to 52 weeks to evaluate the effect of Vedolizumab on maintaining disease remission. It was found that patients in the Vedolizumab treatment group had significantly higher clinical remission rates and clinical response rates compared to the placebo group. AJM300 is another anti-adhesion molecule with broad anti-alpha4 integrin effects. 2009 a multicenter, double-blind, placebo-controlled clinical trial found that high doses of AJM300 significantly reduced disease activity in patients with active Crohn’s disease; in 2014, the company that developed AJM300 again released clinical phase IIa data on AJM300 for the treatment of ulcerative colitis. clinical phase IIa data, showing the same efficacy in ulcerative colitis. Although AJM300 holds promise for the treatment of inflammatory bowel disease, further clinical studies are needed to validate it. It is believed that the adhesion molecule pathway will provide more targets for the development of therapeutic drugs for Crohn’s disease, and more anti-adhesion molecule drugs will certainly be put into clinical research of Crohn’s disease. (ii) Anti-interleukin 12/23 (IL-12/23) drugs IL-12 and IL-23 are cytokines with pro-inflammatory properties that regulate Th1-type cell responses and assist in macrophage recruitment, which are involved in the pathogenesis of Crohn’s disease. In 2012, a clinical trial IIb included 526 patients who were not responding to classical gram therapy and were randomized to placebo treatment and intravenous ustekinumab at 1 mg/kg, 3 mg/kg, and 6 mg/kg, and found a significant response in the 6 mg/kg group at week 6. Treatment was significantly responsive. During the maintenance phase, patients were again randomized to receive placebo or subcutaneous euthyroxamab, and at week 22 the clinical remission and treatment response rates were significantly higher in the euthyrox subcutaneous treatment group than in the placebo control group. A clinical phase III trial of utek for the treatment of Crohn’s disease is currently underway and may provide a new option in the future for patients who have failed to respond to TNF monotherapy. (iii) Chemokine antagonists Chemokines are able to bind to G protein-coupled transmembrane receptors and regulate the recruitment and migration of local leukocytes in the intestinal mucosa, which are involved in the pathogenesis of inflammatory bowel disease. One study found that chemokine receptor 9 is aberrantly expressed in both the small intestine and colon in Crohn’s disease. a 2013 randomized double-blind placebo-controlled study focused on an oral chemokine receptor 9 inhibitor, CCX282-B or Vercirnon. 436 patients with Crohn’s disease first received 12 weeks of placebo or CCX282-B induction therapy, with a treatment response rate of 47% in the placebo group at week 12 compared to 61% in the 500 mg CCX282-B oral treatment group; at week 52 of maintenance therapy, the disease remission rate was 47% in the CCX282-B treatment group compared to 31% in the placebo treatment group. Patients tolerated CCX282-B well throughout the course of treatment. In November, clinical phase III results on the use of this drug in patients with moderately severe active Crohn’s were published in the journal Aliment Pharmacol Ther. The study included 608 patients randomized to placebo, once-daily and twice daily 500 mg vercirnon therapy. The final results failed to confirm the drug’s role in inducing remission, and further validation is needed to determine whether it is effective in maintaining remission. In addition to the above drugs that have entered late stage clinical trials, there are a number of drugs that are in the early stages of research but have shown better promise in the treatment of Crohn’s disease. 1) Anti-interleukin-6 (IL-6) drugs/tocilizumab IL-6 is a cytokine secreted by a variety of immune and non-immune cells that activates immunity and participates in the acute phase response of the body. Tocilizumab is a human monoclonal antibody that inhibits the activation of membrane-bound and soluble IL-6 receptors. A randomized controlled study that included only 36 patients with active Crohn’s disease initially showed the efficacy of tolimumab in Crohn’s disease, but further clinical trials with large samples are needed to confirm this. Studies of other anti-IL-6 agents such as BMS-954429 and PF-04236921 are also in progress. 2) Raquinimod Raquinimod is a new synthetic oral drug that can be used to treat multiple sclerosis. A preliminary clinical phase IIa trial in 2013 enrolled 180 patients with moderately to severely active Crohn’s disease, randomized to placebo, 0.5 mg/day, 1 mg/day, 1.5 mg/day, and 2 mg/day of laquinimod. Patients on the lowest dose of laquinimod showed significant efficacy, including a significant reduction in disease scores and a significant downregulation of fecal calprotectin levels. However, these results need to be further studied. The results of a recent multicenter, double-blind, randomized controlled clinical phase II trial published in the journal GUT in August of this year found that laquinimod had an excellent safety and tolerability profile and was effective in inducing disease remission. 3) Stem cell therapy The use of stem cell transplantation for the treatment of Crohn’s disease has not been conclusively established, and previous studies have mostly been case reports of small samples. The only randomized controlled study so far included only 45 patients with severe Crohn’s disease. Preliminary results showed a reduction in disease activity in patients who received hematopoietic stem cell transplantation, but cytotoxic drugs are administered prior to stem cell transplantation, so the associated risks and benefits still need to be further measured. Another type of MSC from bone marrow and adipose tissue has also received attention. Both clinical phase I and clinical phase II trials have initially demonstrated the efficacy of local injection of MSCs in fistulizing Crohn’s disease, including anal fistula. As for patients with refractory Crohn’s disease, a multicenter, non-blinded, non-randomized clinical phase II trial enrolled 16 Crohn’s disease patients who had failed to respond to TNF monotherapy and were given intravenous MSC infusions, which ultimately yielded highly significant results. Nevertheless, hematopoietic stem cells and MSCs still need to be further investigated in depth. Conclusion: There is no doubt that many of the new drugs currently under investigation will likely be introduced to the market in the future, further increasing our options for treatment of the disease and enabling more patients with Crohn’s disease to better manage their disease and achieve a good quality of life.