Reaction SMILES: [CH3:1]CCCCCCC/C=C\CCCCCCCC(OCC(OC(CCCCCCC/C=C\CCCCCCCC)=O)C[N+](CCNC(C(NCCCN)CCCNCCCN)=O)(C)C)=O.CC1(C)S[C@@H]2[C@H](NC(CC3C=CC=CC=3)=O)C(=O)N2[C@H]1C([O-])=O.[K+].C[C@@H]1O[C@@H](O[C@H]2[C@H](O)[C@@H](O)[C@H](NC(N)=N)[C@@H](O)[C@@H]2NC(N)=N)[C@H]([O:114][C@@H:115]2[O:120][C@@H:119]([CH2:121][OH:122])[C@H:118]([OH:123])[C@@H:117]([OH:124])[C@@H:116]2[NH:125]C)[C@@]1(O)C=O.CC(O)[C@H]1O[C@H](O[C@H:139]2[C@H:144]([OH:145])[C@@H:143]([O:146][C@@H:147]3[O:152][CH2:151][C@:150]([OH:154])([CH3:153])[C@@H:149]([NH:155][CH3:156])[C@@H:148]3[OH:157])[C@H:142]([NH2:158])[CH2:141][C@@H:140]2[NH2:159])[C@H](N)[C@@H](O)[C@@H]1O.OS(O)(=O)=O.OS(O)(=O)=O>>[CH3:1][C@@H:121]([OH:122])[C@H:119]1[O:120][C@H:115]([O:114][C@H:139]2[C@H:144]([OH:145])[C@@H:143]([O:146][C@H:147]3[O:152][CH2:151][C@@:150]([OH:154])([CH3:153])[C@H:149]([NH:155][CH3:156])[C@H:148]3[OH:157])[C@H:142]([NH2:158])[CH2:141][C@@H:140]2[NH2:159])[C@H:116]([NH2:125])[C@@H:117]([OH:124])[C@@H:118]1[OH:123]
Reactant: CN[C@@H]1[C@H](O[C@H]2[C@H](O[C@H]3[C@H](O)[C@@H](O)[C@H](NC(=N)N)[C@@H](O)[C@@H]3NC(=N)N)O[C@@H](C)[C@]2(O)C=O)O[C@@H](CO)[C@H](O)[C@H]1O
Reactant: CCCCCCCC/C=C\CCCCCCCC(=O)OCC(C[N+](C)(C)CCNC(=O)C(CCCNCCCN)NCCCN)OC(=O)CCCCCCC/C=C\CCCCCCCC
Reactant: CN[C@H]1[C@H](O)[C@H](O[C@@H]2[C@@H](O)[C@H](O[C@H]3O[C@H](C(C)O)[C@@H](O)[C@H](O)[C@H]3N)[C@@H](N)C[C@H]2N)OC[C@@]1(C)O
Agent: CC1(C)S[C@@H]2[C@H](NC(=O)Cc3ccccc3)C(=O)N2[C@H]1C(=O)[O-]
Agent: O=S(=O)(O)O
Agent: [K+]
Product: CN[C@@H]1[C@@H](O)[C@@H](O[C@@H]2[C@@H](O)[C@H](O[C@H]3O[C@H]([C@@H](C)O)[C@@H](O)[C@H](O)[C@H]3N)[C@@H](N)C[C@H]2N)OC[C@]1(C)O

Procedure:
The in vitro S1P1 agonist activity of the compound of the present invention was evaluated by the increase in the functional bonding activity into the G-Protein of a GTP[γ-35S] using the membrane of a human S1P1 expressing cell. A cDNA encoding a human S1P1 was cloned from a human colorectal cDNA library, and introduced to an expression vector pcDNA3.1 to construct a S1P1-pcDNA3.1. Then, by Lipofectamine 2000 (GIBCO), the S1P1-pcDNA3.1 was transfected into a CHO cell, and cultured in a Ham's F-12 culture medium containing 10% fetal bovine serum, 100 U/mL Penicillin, 100 μg/mL Streptomycin, and 1 mg/mL G418 disulfate, to obtain a stable, G418-resistant strain. The cultured human S1P1 expressing cells were isolated in a 1 mM EDTA/2Na-containing PBS, and disrupted under ice-cooling by a homogenizer made of glass in a 1 mM Tris HCl (pH 7.4) buffer solution containing 0.1 mM EDTA and a protein inhibitor. It was centrifuged at 1,400×10 min, and a supernatant was further centrifuged at 4° C. for 60 min at 100,000×g, and suspended in a 10 mM Tris HCl (pH 7.4) buffer solution containing 1 mM EDTA. The obtained membrane (0.13 mg/mL) and 50 pM GTP[γ-35S] (NEN; inactive 1250 Ci/mmol) were reacted in a 20 mM HEPES (pH 7.0) buffer solution (total amount: 150 μL) containing 100 mM NaCl, 10 mM MgCl2, 0.1% fatty acid-free BSA, and 5 μM GDP for 1 hour together with the compound of the present invention (10−12 to 10−5 M), and then a membrane was recovered on a GF-C plate with a Cell Harvester (Packard, FilterMate). The FilterMate was dried at 50° C. for 60 min, and Microscinti-o (Packard) was added thereto for measurement by a liquids scintillation counter for a microplate (Packard, TOP count). For evaluation of the human S1P1 agonist activity of the compound of the present invention and the comparative compound, the percentages with the rate of a maximum reaction to make the GTP[γ-35S] bonds saturated in the presence of the compound being set at 100%, and the rate of the reaction of the GTP[γ-35S] bonds in the absence of the compound being set at 0% was used, a non-linear regression curve was plotted, and a concentration to cause an agonist activity operating 50% of the maximum reaction was defined as an EC50 value (nM).