mip-1α

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。

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-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).

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-1072 is the prostate-specific membrane antigen inhibitor.

MIP-1095 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.

Met-RANTES (human) acetate 为Met-RANTES (human)的醋酸盐版本，它是CCR1和CCR5的有效拮抗剂。该化合物能够抑制人类趋化因子MIP-1α和MIP-1β，其IC50值分别为5 nM和2 nM。此外，Met-RANTES (human) acetate 也能减缓骨质破坏及缓解大鼠佐剂诱导的关节炎(AIA)的症状。

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。

Fuscin is a quinonoid fungal metabolite originally isolated from O. fuscum that has diverse biological activities. It inhibits binding of the ADP/ATP translocase inhibitor atractyloside to rat liver mitochondria in an ADP-dependent manner when used at a concentration of 50 μM in a radioligand binding assay. Fuscin (20 μM) reduces the glutathione content of rat liver mitochondria to 28% of controls and inhibits NADH oxidation in sonicated pigeon heart mitochondria preparations in a concentration-dependent manner. It competes with macrophage inflammatory protein 1α (MIP-1α) for binding to CCR5 chemokine receptors in vitro with an IC50 value of 21 μM.

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。

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。