Acetamide, N-[2-[(5-chloro-2 methoxyphenyl)amino]-4'-methyl[4,5'-bithiazol]-2'-yl]-inhibits pro-matrix metalloproteinase activation and can be used to prevent, treat or ameliorate MMP9 and/or MMP13-mediated syndromes.

BPHA (MMP-2/MMP-9 Inhibitor II) is a potent, selective and orally active inhibitor of MMP-2, MMP-9 and MMP-14 with IC50s of 12 nM, 16 nM and 17 nM, respectively.BPHA does not inhibit MMP-1, -3 and -7 (IC50s of 974, >1000 and 795 nM, respectively).BPHA has anti-angiogenic and BPHA has anti-angiogenic and anti-tumor activities.

MMP-9-IN-6 is an MMP-9 inhibitor with an IC50 value of 50 μM and good anti-ulcer efficacy.MMP-9-IN-6 has potential anti-tumor activity and can be used to study tissue remodeling, wound repair and atherosclerosis.

MMP-9-IN-8 (Compound 3), an MMP-9 inhibitor, exhibits inhibitory activities of 42.16% at 10 μM and 58.28% at 50 μM. Additionally, MMP-9-IN-8 demonstrates anti-cancer properties, inducing apoptosis in MCF-7 cells with an IC50 value of 23.42 μM [1].

MMP-9-IN-5 is an MMP-9 inhibitor with an IC50 value of 4.49 nM and is able to form hydrogen bonds with MMP-9. MMP-9-IN-5 also inhibits AKT activity with an IC50 value of 1.34 nM. MMP-9-IN-5 exhibits cytotoxicity, induces apoptosis and can be used in cancer research.

MMP-9/MMP-13 Inhibitor I is a dual inhibitor of MMP-9 and MMP-13 with IC50 of both 0.9 nM. MMP-9/MMP-13 Inhibitor I is over 20 times more selective for MMP-9/MMP-13 than other MMPs.

MMP-2/MMP-9-IN-1 is a potent, highly selective and orally bioavailable inhibitor of type IV collagenases (MMP-9 and MMP-2) with an IC50 of 0.24 and 0.3 1 μM for MMP-9 and MMP-2, respectively. activity, which can be used to study cancer.

MMP-9-IN-4 is an inhibitor of MMP-9 and interacts with MMP-9 to form H-π with an IC50 value of 7.46 nM. MMP-9-IN-4 also inhibits AKT activity with an IC50 value of 8.82 nM. MMP-9-IN-4 induces apoptosis, shows cytotoxicity and can be used to study Cancer.

MMP-9-IN-3 is an MMP-9 inhibitor (IC50: 5.56 nM) that forms hydrogen bonds with MMP-9. MMP-9-IN-3 inhibits AKT activity (IC50: 2.11 nM). mmp-9-IN-3 is cytotoxic and induces apoptosis. mmp-9-IN-3 can be used to study cancer.

MMP-2/9-IN-1 (Compound 4a) is a potent dual inhibitor of MMP-2 (IC50: 56 nM) and MMP-9 (IC50: 38 nM). leading to DNA fragmentation.

MMP-9 inhibitor I is an inhibitor of matrix metalloproteinase-9 (MMP-9) that is selective over MMP-1 and MMP-13 (IC50s = 5, 1,050, and 113 nM, respectively). It also decreases the activity of TNF-α converting enzyme (TACE) in a dose-dependent manner (IC50 = 0.54 μM). MMP-9 inhibitor I decreases TNF-α secretion stimulated by LPS in BV-2 microglial cells when used at concentrations of 50 and 100 μM.

MMP-9-IN-1 is an inhibitor of specific matrix metalloproteinase-9 (MMP-9).

Astragaloside IV (AS-IV), an active component isolated from Astragalus membranaceus, suppresses the activation of ERK1/2 and JNK, and downregulates matrix metalloproteases (MMP)-2, (MMP)-9 in MDA-MB-231 breast cancer cells. Astragaloside IV is a bioactive saponin first isolated from the dried plant roots of the genus Astragalus, which is used in traditional Chinese medicine.1 It dose-dependently inhibits human adenovirus type 3 (HAdV-3) in A549 cells (IC50 = 23 μM; LC50 = 865 μM).It inhibits replication of HAdV-3 and decreases HAdV-3-induced apoptosis. It has diverse protective effects for the cardiovascular, immune, digestive, and nervous systems. In particular, it reduces myocardial infarct size in dogs when administered prior to coronary ligation and reduces reperfusion arrhythmias in isolated rat hearts.

Histatin 5 acetate inhibits the activity of the host matrix metalloproteinases MMP-2 and MMP-9 with IC50s of 0.57 and 0.25 μM, respectively.

CTTHWGFTLC, CYCLIC acetate is an inhibitor for matrix metalloproteinases (MMP)-2 and MMP-9. It is also called type IV collagenase or gelatinase. Gelatinases are potential targets of therapeutic intervention in cancer, and inhibitors of these enzymes can prevent tumor progression.

Norepinephrine (Levophed) can stimulate apoptosis in adult rat ventricular myocytes by activation of the β-adrenergic pathway. It can up-regulate the expression of vascular endothelial growth factor, matrix metalloproteinase (MMP)-2, and MMP-9 in nasopharyngeal carcinoma tumour cells.

Batimastat (BB94) (BB-94) is an effective, broad-spectrum matrix metalloprotease (MMP) inhibitor. Batimastat induces extracellular matrix degradation and inhibits angiogenesis, tumor growth and invasion, and metastasis.

Ethyl gallate (gallic acid ethyl ester) obviously decreases cell proliferation in MDA-MB-231 and MCF-7 cells in a dose- and time-dependent manner, exhibits cytotoxicity in a dose-dependent manner. Ethyl gallate can inhibit the abilities of invasion of breast cancer in vitro by inhibiting the mRNA levels of MMP-9/MMP-2, phosphorylation of Akt and protein expression of NF-κB and inhibits hydrogen peroxide signaling, may represent an alternative class of vasopressors for use in septic shock. Also, Ethyl gallate suppresses proliferation and invasion in human breast cancer cells by modulating the PI3K/Akt pathway, which may contribute to inhibiting their downstream targets such as NF-κB p-65, Bcl-2/Bax, and mRNA levels of MMP-2 and MMP-9 in breast cancer cells, could be used as potential antioxidants with safe therapeutic application in cancer chemotherapy.

Ilomastat (GM6001) (GM6001, Galardin) is a broad spectrum matrix metalloprotease (MMP) inhibitor.

Arg-Gly-Asp-Ser is an integrin-binding sequence that inhibits integrin receptor function. It decreases systemic inflammation via inhibition of collagen-triggered activation of leukocytes and attenuates expression of inflammatory cytokines, MMP-9, and iNOS

SB-3CT is a potent and specific gelatinase inhibitor for MMP-2(Ki=13.9 nM) and MMP-9(Ki=600 nM).

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.

Edaravone (MCI-186)(MCI-186) is a potent new free radical scavenger used for the therapy of patients with acute brain infarction.

1. 6-Shogaol (6-Shogaol) has antipyretic and analgesic effects in addition to inhibitory effect on lipoxygenase activity. 2. 6-shogaol has anti-inflammatory property, reduces the inflammatory response and protected the femoral cartilage from damage produced in a CFA monoarthritic model of the knee joint of rats. 3. 6-Shogaol inhibits the growth of human cancer cells and induces apoptosis in COLO 25 cells through modulation of mitochondrial functions regulated by reactive oxygen species (ROS). 4. 6-Shogaol effectively inhibit invasion and metastasis of hepatocellular carcinoma through diverse molecular mechanisms, including inhibition of the MAPK and PI3k/Akt pathways and NF-κB and STAT3 activities to suppress expression of MMP-2/-9 and uPA and block angiogenesis, could further regulate urokinase-type plasminogen activity.

This cyclic CTT Gelatinase Inhibitor peptide is an inhibitor for matrix metalloproteinases (MMP)-2 and MMP-9. It is also called type IV collagenase or gelatinase. Gelatinases are potential targets of therapeutic intervention in cancer, and inhibitors of t

Histatin 5 (TFA)(115966-68-2,free) (Histatin 5 (TFA)) inhibits the activity of the host matrix metalloproteinases MMP-2 and MMP-9 with IC50s of 0.57 and 0.25 μM, respectively.

Inostamycin A is a bacterial metabolite that has been found inStreptomycesand has anticancer activity.1It is an inhibitor of CDP-diacylglycerol:inositol 3-phosphatidyltransferase (IC50= 0.02 μg/ml in A431 cell membranes) and is selective for CDP-diacylglycerol:inositol 3-phosphatidyltransferase over phospholipase C (PLC) and phosphatidylinositol kinase at 10 μg/ml.2Inostamycin A decreases viability of YCU-T892, KCC-TC873, KB, HSC-4, and YCU-T891 oral squamous cell carcinoma (OSCC) cells in a concentration-dependent manner.3It induces cell cycle arrest in the G1phase in HSC-4 cells when used at a concentration of 250 ng/ml and induces apoptosis in Ms-1 small cell lung cancer cells at 300 ng/ml.3,4Inostamycin A also reduces levels of matrix metalloproteinase-2 (MMP-2) and MMP-9 and inhibits EGF-induced migration of HSC-4 cells.5 1.Imoto, M., Umezawa, K., Takahashi, Y., et al.Isolation and structure determination of inostamycin, a novel inhibitor of phosphatidylinositol turnoverJ. Nat. Prod.53(4)825-829(1990) 2.Imoto, M., Taniguchi, Y., and Umezawa, K.Inhibition of CDP-DG: inositol transferase by inostamycinJ. Biochem.112(2)299-302(1992) 3.Baba, Y., Tsukuda, M., Mochimatsu, I., et al.Cytostatic effect of inostamycin, an inhibitor of cytidine 5'-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG): inositol transferase, on oral squamous cell carcinoma cell linesCell Biol. Int.25(7)613-620(2001) 4.Imoto, M., Tanabe, K., Simizu, S., et al.Inhibition of cyclin D1 expression and induction of apoptosis by inostamycin in small cell lung carcinoma cellsJpn. J. Cancer Res.89(3)315-322(1998) 5.Baba, Y., Tsukuda, M., Mochimatsu, I., et al.Inostamycin, an inhibitor of cytidine 5'-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG): Inositol transferase, suppresses invasion ability by reducing productions of matrix metalloproteinase-2 and -9 and cell motility in HSC-4 tongue carcinoma cell lineClin. Exp. Metastasis18(3)273-279(2000)

Phytolaccaceae has anti-tumor activity, the mechanism may be related to the capacity of Esculentoside H for TNF release.

Lucideric acid A (Lucidenic acid A) is a modulator of JNK and p38 and enhances LPS-induced immune responses in monocytic THP-1 cells possibly via the modulation of p38 and JNK/MAPKs activation.

Total panax notoginsenosides (TPNS) are the main active ingredients in San-Chi, the root of(Burk) F.H. Chen, which belongs to the Araliaceae family and has been used in traditional Chinese medicine to treat atherosclerosis;TPNS can prevent atherosclerosis

Glaucine has antitussive, antioxidative potential and antiviral activities, it may be an anti-arthritic agent, it can enhance LPS and zymosan-induced IL-10 production. Glaucine can inhibit the migration and invasion of human breast cancer cells by MMP-9 i

SH491 (Compound 33) serves as an antiosteoporosis agent, effectively inhibiting RANKL-induced osteoclast differentiation in bone-marrow-derived monocytes (BMMs) with an IC50 of 11.8 nM. Additionally, SH491 suppresses the expression of genes and proteins related to osteoclastogenesis, specifically TRAP, CTSK, MMP-9, and ATPase v0d2 [1].

Histatin 5 inhibits the activity of the host matrix metalloproteinases MMP-2 and MMP-9 with IC50s of 0.57 and 0.25 μM, respectively. Histatin 5 is a human basic salivary peptide with strong fungicidal properties in vitro.

Funalenone is a phenalenone originally isolated from A. niger. It inhibits HIV-1 integrase (IC50 = 10 μM) and HIV-1 replication in human peripheral blood cells transformed by murine leukemia virus (HPB-M(a); IC50 = 1.7 μM) but is less cytotoxic to mammalian HPB-M(a) cells (IC50 = 87 μM). Funalenone selectively inhibits matrix metalloproteinase-1 (MMP-1; IC50 = 170 μM) over MMP-2 and MMP-9, which it inhibits by 18.3 and 38.2%, respectively, when used at a concentration of 400 μM. It also inhibits the bacterial cell wall synthesis enzymes MraY and MurG (IC50s = 25.5 μM in a membrane plate assay) and inhibits growth of S. aureus with a MIC value of 64 μg/mL.

The NF-κB Activation Inhibitor III, controls the biological activity of NF-κB. It is primarily used for Inflammation/Immunology applications.

IVMT-Rx-3 is a chemical compound that serves as an inhibitor of SDCBP's targeting of the PDZ1 and PDZ2 domains of MDA-9/Syntenin. It effectively blocks the MDA-9/Syntenin-Src interaction, diminishes NF-κB activation, and suppresses MMP-2/MMP-9 expression, thereby inhibiting melanoma metastasis [1].

Lucidenic acid C has anti-invasive effect, it shows significant inhibitory effects on PMA-induced MMP-9 activity and invasion of HepG(2 )cells.

Edaravone, a novel and potent free radical scavenger, effectively prevents MMP-9-related brain hemorrhage in rats treated with tissue plasminogen activator. Its deuterium-labeled variant, Edaravone D5, retains the original compound's attributes while offering isotopic labeling benefits.

Rebimastat is a sulfhydryl-based second-generation matrix metalloproteinase (MMP) inhibitor with potential antineoplastic activity. Rebimastat selectively inhibits several MMPs (MMP 1, 2, 8, 9, and 14), thereby inducing extracellular matrix degradation, and inhibiting angiogenesis, tumor growth and invasion, and metastasis.

22-(4′-py)-JA, a semisynthetic derivative of junamycin A isolated from the Thai blue sponge (Xestospongia sp.), exhibits antimetastatic properties by inhibiting the AKT/mTOR/p70S6K signaling pathway. It also impedes tumor cell invasion and angiogenesis in human umbilical vein endothelial cells (HUVEC), while suppressing the expression of metalloproteinases (MMP-2 and MMP-9), hypoxia-inducible factor 1α (HIF-1α), and vascular endothelial growth factor (VEGF). Its potent anticancer activity is particularly noted against non-small cell lung cancer (NSCLC) [1].

Coenzyme Q0 (CoQ0), a potent, orally active ubiquinone compound derived from Antrodia cinnamomea, induces apoptosis and autophagy. It suppresses HER-2/AKT/mTOR signaling, enhancing apoptosis and autophagy mechanisms. Additionally, Coenzyme Q0 regulates NFκB/AP-1 activation and promotes Nrf2 stabilization, contributing to the attenuation of inflammation and redox imbalance. It also exhibits anti-angiogenic activity by downregulating MMP-9/NF-κB and upregulating HO-1 signaling.

Hepcidin-1 (mouse) is a peptide hormone that regulates iron balance, elevates mRNA for TRAP, cathepsin K, and MMP-9, and promotes TRAP-5b protein secretion. This compound also reduces FPN1 protein levels and boosts intracellular iron, ultimately aiding in osteoclast differentiation [1].

ExcisaninA may be a potent inhibitor of AKT signaling pathway in tumor cells, it can inhibit invasion by suppressing MMP-2 and MMP-9 expression, it may be a potential anti-metastatic chemotherapeutic agent for the treatment of breast cancer. Excisanin A shows comparable inhibitory effects on the LPS-induced production of NO and PGE2, and activation of NF-kappaB without affecting cell viability.Excisanin A induces apoptosis in colon cancer cell line SW620 as determined by Annexin V staining, the cleavage of caspase-3 and the proteolytic degradation of poly (ADP-ribose) polymerase (PARP).

Dnp-PLGMWSR is a fluorogenic substrate for matrix metalloproteinase-2 (MMP-2) and MMP-9. The activity of MMP-2 and MMP-9 can be quantified by measuring tryptophan fluorescence that is unquenched upon peptide hydrolysis that removes the N-terminal dinitrophenol (Dnp) group.

Aminopeptidase N (AP-N) inhibitor is a reversible inhibitor of AP-N/CD13 (IC50 = 25 μM). It is selective for AP-N/CD13 over matrix metalloproteinase-9 (MMP-9), angiotensin converting enzyme (ACE), neutral endopeptidase (NEP), γ-glutamyl transpeptidase, and the serine proteases dipeptidyl peptidase 4 (DPP-4) and cathepsin G at a concentration of 1 mM. AP-N inhibitor is non-cytotoxic to U937 cells at a concentration of 100 μM.

Histatin 5 TFA effectively inhibits host matrix metalloproteinases (MMP-2) and (MMP-9), demonstrating inhibition concentrations (IC 50s) of 0.57 μM and 0.25 μM, respectively.

VPLSLYSG, an octapeptide susceptible to degradation by matrix metalloproteinase-9 (MMP-9), MMP-1, and MMP-2, holds potential applications as an MMP substrate [1] [2] [3].

Rac)-Tanomastat ((Rac)-BAY 12-9566) is a racemate of Tanomastat. Tanomastat (BAY 12-9566) is an orally active, zinc carboxy-containing inhibitor of non-peptide biphenyl matrix metalloproteinases (MMPs) that inhibits MMP-2 (Ki: 11 nM), MMP-3 (Ki: 143 nM), MMP-9 (Ki: 301 nM), and MMP-13 (Ki: 1470 nM). In several experimental tumour models, Tanomastat exhibits anti-invasive and anti-metastatic effects.

ND-336 is a highly selective inhibitor ofMMP-2, MMP-9 and MMP-14. ND-336 accelerates diabetic wound healing by lowering inflammation and by enhancing angiogenesis and re-epithelialization of the wound.

FAK-IN-3 is a potent inhibitor of adherens spot kinase (FAK). FAK-IN-3 reduces migration and invasion of PA-1 cells and inhibits the expression of MMP-2 and MMP-9. FAK-IN-3 inhibits tumor growth and metastasis with no significant adverse effects. FAK-IN-3 has shown investigational potential in ovarian cancer.