mip 1

Mip-IN-1（S,S-28i）是一款新型雷帕霉素衍生的Mip抑制剂，对Neisseria meningitidis和Neisseria gonorrhoeae的Mip蛋白具有高效的抗酶作用，能显著增强巨噬细胞杀灭细菌的能力。

Maraviroc (Selzentry) 是一种 C-C 趋化因子受体 5 拮抗剂，具有抑制HIV 的活性。

TAK-220 is a selective and orally bioavailable CCR5 antagonist (IC50s: 3.5 nM and 1.4 nM for inhibition on the binding of RANTES and MIP-1α to CCR5, respectively).

BX471 hydrochloride (ZK-811752 hydrochloride) is a potent, selective non-peptide CCR1 antagonist (Ki: 1 nM for human CCR1). It shows 250-fold selectivity for CCR1 over CCR2, CCR5, and CXCR4.

TAK-779 (Takeda 779) 是一种非肽类CCR5和CXCR3 拮抗剂，对CCR5的Ki 值为 1.1 nM，并选择性抑制R5 HIV-1。

MIP-1095 is the prostate-specific membrane antigen inhibitor.

MIP-1072 is the prostate-specific membrane antigen inhibitor.

MIP-1095 I-131 is a small molecule PSMA inhibitor.

MIP-1095 I-123, as a radiotracer, is under investigation in clinical trial NCT00712829 (Evaluating the Safety, Pharmacokinetics, Tissue Distribution, Metabolism and Dosimetry of Two Prostate Cancer Imaging Agents).

MLN-3897 (CCR1 antagonist 10) 是一种具有口服活性的 CCR1 拮抗剂，对于 125I-MIP-1α 与 THP-1 细胞膜的结合，Ki 为 2.3 nM。 MLN-3897 抑制 Akt 信号转导和 MM 细胞存活和增殖。

Talabostat (PT100, Val-boroPro) is a potent, nonselective and orally available dipeptidyl peptidase IV (DPP-IV) inhibitor with a Ki of 0.18 nM. Talabostat is a nonselective DPP-IV inhibitor, inhibiting DPP8 9, FAP, DPP2 and some other DASH family enzymes essentially as potently as it inhibits DPP-IV[1]. Talabostat stimulates the immune system by triggering a proinflammatory form of cell death in monocytes and macrophages known as pyroptosis. The inhibition of two serine proteases, DPP8 and DPP9, activates the proprotein form of caspase-1 independent of the inflammasome adaptor ASC[2]. Talabostat competitively inhibits the dipeptidyl peptidase (DPP) activity of FAP and CD26 DPP-IV, and there is a high-affinity interaction with the catalytic site due to the formation of a complex between Ser630 624 and the boron of talabostat[3]. Talabostat can stimulate immune responses against tumors involving both the innate and adaptive branches of the immune system. In WEHI 164 fibrosarcoma and EL4 and A20 2J lymphoma models, PT-100 causes regression and rejection of tumors. The antitumor effect appears to involve tumor-specific CTL and protective immunological memory. Talabostat treatment of WEHI 164-inoculated mice increases mRNA expression of cytokines and chemokines known to promote T-cell priming and chemoattraction of T cells and innate effector cells[3]. Talabostat treated mice show significant less fibrosis and FAP expression is reduced. Upon PT100 treatment, significant differences in the MMP-12, MIP-1α, and MCP-3 mRNA expression levels in the lungs are also observed. Treatment with PT100 in this murine model of pulmonary fibrosis has an anti-fibro-proliferative effect and increases macrophage activation[4]. [1]. Connolly BA, et al. Dipeptide boronic acid inhibitors of dipeptidyl peptidase IV: determinants of potencyand in vivo efficacy and safety. J Med Chem. 2008 Oct 9;51(19):6005-13. [2]. Okondo MC, et al. DPP8 and DPP9 inhibition induces pro-caspase-1-dependent monocyte and macrophage pyroptosis. Nat Chem Biol. 2017 Jan;13(1):46-53. [3]. Adams S, et al. PT-100, a small molecule dipeptidyl peptidase inhibitor, has potent antitumor effects and augments antibody-mediated cytotoxicity via a novel immune mechanism. Cancer Res. 2004 Aug 1;64(15):5471-80. [4]. Egger C, et al. Effects of the fibroblast activation protein inhibitor, PT100, in a murine model of pulmonary fibrosis. Eur J Pharmacol. 2017 Aug 15;809:64-72.

MLN-3897 TFA 是一种有效的CCR1 拮抗剂，对 125I-MIP-1α 与 THP-1 细胞膜的结合具有抑制作用。

trans-J-113863为一种高效的CCR1及CCR3受体拮抗剂，能够抑制MIP-1α对CCR1的趋化作用和eotaxin对CCR3的趋化作用，IC50值分别为9.57和93.8 nM。

TLR4agonist-1 (TEA) (compound 17a)为Toll-like Receptor 4 (TLR4)的高效激动剂，在RAW 264.7及MM6细胞中能有效促进MIP-1β的生成。

TLR4agonist-1 (compound 17a)是一种针对Toll-like Receptor 4 (TLR4)的高效激动剂，能有效激发RAW 264.7与MM6细胞产生MIP-1β。

β-Defensin-2 is a peptide with antimicrobial properties that protects the skin and mucosal membranes of the respiratory, genitourinary, and gastrointestinal tracts.1It inhibits the growth of periodontopathogenic and cariogenic bacteria, includingP. gingivalisandS. salivarius.2β-Defensin-2 (30 μg/ml) stimulates gene expression and production of IL-6, IL-10, CXCL10, CCL2, MIP-3α, and RANTES by keratinocytes.3It also stimulates calcium mobilization, migration, and proliferation of keratinocytes when used at concentrations of 30, 10, and 40 μg/ml, respectively. β-Defensin-2 induces IL-31 production by human peripheral blood-derived mast cellsin vitrowhen used at a concentration of 10 μg/ml and by rat mast cellsin vivofollowing a 500 ng intradermal dose.4Expression of β-defensin-2 is increased in psoriatic skin and chronic wounds.5,6 1.Lehrer, R.I.Primate defensinsNat. Rev. Microbiol.2(9)727-738(2004) 2.Ouhara, K., Komatsuzawa, H., Yamada, S., et al.Susceptibilities of periodontopathogenic and cariogenic bacteria to antibacterial peptides, β-defensins and LL37, produced by human epithelial cellsJ. Antimicrob. Chemother.55(6)888-896(2005) 3.Niyonsaba, F., Ushio, H., Nakano, N., et al.Antimicrobial peptides human β-defensins stimulate epidermal keratinocyte migration, proliferation and production of proinflammatory cytokines and chemokinesJ. Invest. Dermatol.127(3)594-604(2007) 4.Niyonsaba, F., Ushio, H., Hara, M., et al.Antimicrobial peptides human β-defensins and cathelicidin LL-37 induce the secretion of a pruritogenic cytokine IL-31 by human mast cellsJ. Immunol.184(7)3526-3534(2010) 5.Huh, W.-K., Oono, T., Shirafuji, Y., et al.Dynamic alteration of human β-defensin 2 localization from cytoplasm to intercellular space in psoriatic skinJ. Mol. Med. (Berl.)80(10)678-684(2002) 6.Butmarc, J., Yufit, T., Carson, P., et al.Human β-defensin-2 expression is increased in chronic woundsWound Repair Regen.12(4)439-443(2004)

Lugdunin是一种具有抗菌活性的肽类抗生素。该化合物能够通过破坏细菌细胞膜的电位来抑制革兰氏阳性菌的生长，特别是对金黄色葡萄球菌（Staphylococcus aureus）表现出高效能，有效降低其在皮肤和鼻腔的定植能力。此外，Lugdunin还能在人类角质形成细胞和小鼠皮肤中促进LL-37和CXCL8 MIP-2的表达。

Nagrestipen 是一种人巨噬细胞炎症蛋白-1α 变体，也称为 ECI 301，主要用于癌症、肿瘤、转移、放射肿瘤学以及肿瘤转移研究试验，具有显著的抗肿瘤活性。