Drug Information

General Information of This Drug
Drug ID DRG00407
Drug Name Combretastatin A4
Synonyms
Combretastatin A4; 117048-59-6; Combretastatin A-4; Combrestatin A4; (Z)-2-METHOXY-5-(3,4,5-TRIMETHOXYSTYRYL)PHENOL; Combretastatin 4; Combretastatin-A4; CA-4; 2'-deoxycombretastatin A1; NSC-613729; 2-methoxy-5-[(Z)-2-(3,4,5-trimethoxyphenyl)ethenyl]phenol; Crc 87-09; CHEMBL67; MFCD03453309; 3,4,5-Trimethoxy-3'-hydroxy-4'-methoxystilbene; NSC-817373; 16U6OP69RQ; Phenol, 2-methoxy-5-[(1Z)-2-(3,4,5-trimethoxyphenyl)ethenyl]-; CA4; 2-Methoxy-5-[(1Z)-2-(3,4,5-trimethoxyphenyl)ethenyl]phenol; 2-methoxy-5-[(Z)-2-(3,4,5-trimethoxyphenyl)vinyl]phenol; 2-Methoxy-5-[(Z)-2-(3,4,5-trimethoxy-phenyl)-vinyl]-phenol; Phenol, 2-methoxy-5-(2-(3,4,5-trimethoxyphenyl)ethenyl)-, (Z)-; NSC 817373; Crc-98-09; UNII-16U6OP69RQ; combretastin A4; Combrestatin A-4; Combretastin A-4; combretastatin-A-4; Combretastastin A-4; NSC 609397; NSC 613729; 2-methoxy-5-(3,4,5-trimethoxystyryl)phenol; Z-Combretastatin A-4; 2-Methoxy-5-[2-(3,4,5-trimethoxy-phenyl)-vinyl]-phenol; SCHEMBL18945; combretastatin A-4, (CSA4); CA 4; GTPL8854; COMBRETASTATIN A-4 [MI]; CHEBI:181391; DTXSID101025983; GLXC-02861; HMS3650G11; AMY24892; COMBRETASTATIN A4 [WHO-DD]; EX-A4207; HY-N2146; BDBM50005480; s7783; AKOS015950727; AC-5280; CCG-265026; CS-6023; DB14680; DS-5860; Phenol,4,5-trimethoxyphenyl)ethenyl]-; ST-1986; C2520; Combretastatin A4, >=98% (HPLC), powder; NS00116331; 5-(3,4,5-trimethoxystyryl)-2-methoxyphenol; C20268; 3'-Hydroxy-3,4,4',5-tetramethoxy-cis-stilbene; EN300-1587417; (Z)-5-(3,4,5-trimethoxystyryl)-2-methoxyphenol; SR-01000946784; (Z)-3''-hydroxy-3,4,4'',5-tetramethoxystilbene; Q5150955; SR-01000946784-1; BRD-K61195623-001-01-4; Z2312943638; [3,4,5-trimethoxy-3'-hydroxy-4'-methoxy-(z)-stilbene]; 2-Methoxy-5-[(Z)-2-(3,4,5-trimethox y-phenyl)-vinyl]-phenol; (combretastin A-4)2-Methoxy-5-[2-(3,4,5-trimethoxy-phenyl)-vinyl]-phenol; 5-[(S)-2-Hydroxy-2-(3,4,5-trimethoxy-phenyl)-ethyl]-2-methoxy-phenol; (combretastatin A-4)2-Methoxy-5-[2-(3,4,5-trimethoxy-phenyl)-vinyl]-phenol; 1-(3,4,5-Trimethoxyphenyl)-2-(3'-hydroxy-4'-methoxyphenyl) ethane 3,4,5-trimethoxy-3'-hydroxy-4'-methoxystilbene
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Target(s) Microtubule (MT)  Target Info 
Structure
Formula
C18H20O5
#Ro5 Violations (Lipinski): 0 Molecular Weight (mw) 316.3
Lipid-water partition coefficient (xlogp) 3.7
Hydrogen Bond Donor Count (hbonddonor) 1
Hydrogen Bond Acceptor Count (hbondacc) 5
Rotatable Bond Count (rotbonds) 6
PubChem CID
5351344
Canonical smiles
COC1=C(C=C(C=C1)C=CC2=CC(=C(C(=C2)OC)OC)OC)O
InChI
InChI=1S/C18H20O5/c1-20-15-8-7-12(9-14(15)19)5-6-13-10-16(21-2)18(23-4)17(11-13)22-3/h5-11,19H,1-4H3/b6-5-
InChIKey
HVXBOLULGPECHP-WAYWQWQTSA-N
IUPAC Name
2-methoxy-5-[(Z)-2-(3,4,5-trimethoxyphenyl)ethenyl]phenol
The activity data of This Drug
Standard Type Value Disease Model Cell line Cell line ID Ref.
Half Maximal Cytotoxicity Concentration (CC50) 13.9 uM Normal HT22 cell CVCL_0321 [1]
Half Maximal Cytotoxicity Concentration (CC50) 38.3 uM Hepatocellular carcinoma Huh-7 cell CVCL_0336 [2]
Half Maximal Cytotoxicity Concentration (CC50) >300 uM Normal HEK-293T cell CVCL_0063 [3]
Half Maximal Effective Concentration (EC50) 3.45 nM Ovarian serous adenocarcinoma OVCAR-3 cell CVCL_0465 [4]
Half Maximal Effective Concentration (EC50) 3.5 nM Skin squamous cell carcinoma A431 cell CVCL_0037 [5]
Half Maximal Effective Dosage (ED50) 2.7 ug/mL Lymphoma P388 cell CVCL_7222 [6]
Half Maximal Effective Dosage (ED50) 0.03 pM Cutaneous melanoma SK-MEL-5 cell CVCL_0527 [7]
Half Maximal Effective Dosage (ED50) 12:00 PM Colon cancer HT29 cell CVCL_A8EZ [7]
Half Maximal Effective Dosage (ED50) 1.4 uM Cutaneous melanoma SK-MEL-5 cell CVCL_0527 [8]
Half Maximal Effective Dosage (ED50) 5.6 uM Invasive breast carcinoma MCF-7 cell CVCL_0031 [8]
Half Maximal Growth Inhibition (GI50) 0.26 ng/mL Anaplastic thyroid carcinoma SW-1736 cell CVCL_3883 [9]
Half Maximal Growth Inhibition (GI50) 0.34 ug/mL Colon carcinoma KM-20L2 cell CVCL_D889 [10]
Half Maximal Growth Inhibition (GI50) 0.39 ug/mL Pancreatic ductal adenocarcinoma BxPC-3 cell CVCL_0186 [11]
Half Maximal Growth Inhibition (GI50) 0.6 ng/mL Lung large cell carcinoma NCI-H460 cell CVCL_0459 [10]
Half Maximal Growth Inhibition (GI50) 0.65 ng/mL Hypopharyngeal squamous cell carcinoma FaDu cell CVCL_1218 [9]
Half Maximal Growth Inhibition (GI50) 0.8 ng/mL Prostate carcinoma DU145 cell CVCL_0105 [12]
Half Maximal Growth Inhibition (GI50) <1 ug/mL Ovarian serous adenocarcinoma OVCAR-3 cell CVCL_0465 [6]
Half Maximal Growth Inhibition (GI50) <1 ug/mL Glioblastoma SF-295 cell CVCL_1690 [6]
Half Maximal Growth Inhibition (GI50) >1 ng/mL Glioblastoma SF-295 cell CVCL_1690 [10]
Half Maximal Growth Inhibition (GI50) <1 ng/mL Astrocytoma SF268 cell CVCL_1689 [13]
Half Maximal Growth Inhibition (GI50) 2 ug/mL Cutaneous melanoma SK-MEL-5 cell CVCL_0527 [6]
Half Maximal Growth Inhibition (GI50) 2.6 ug/mL Neuroblastoma SK-N-SH cell CVCL_0531 [6]
Half Maximal Growth Inhibition (GI50) 7.1 ug/mL Anaplastic thyroid carcinoma SW-1736 cell CVCL_3883 [6]
Half Maximal Growth Inhibition (GI50) 61 ng/mL Colon carcinoma KM-20L2 cell CVCL_D889 [13]
Half Maximal Growth Inhibition (GI50) <0.1 nM Ovarian serous cystadenocarcinoma SK-OV-3 cell CVCL_0532 [14]
Half Maximal Growth Inhibition (GI50) 1 nM Prostate carcinoma PC-3 cell CVCL_0035 [15]
Half Maximal Growth Inhibition (GI50) 2 nM T acute lymphoblastic leukemia CCRF-CEM cell CVCL_0207 [15]
Half Maximal Growth Inhibition (GI50) 2 nM Renal carcinoma RXF 393 cell CVCL_1673 [15]
Half Maximal Growth Inhibition (GI50) 2 nM Non-small cell lung carcinoma NCI-H522 cell CVCL_1567 [16]
Half Maximal Growth Inhibition (GI50) 2 nM Non-small cell lung carcinoma HOP-62 cell CVCL_1285 [15]
Half Maximal Growth Inhibition (GI50) 2 nM Melanoma M14 cell CVCL_1395 [15]
Half Maximal Growth Inhibition (GI50) 2 nM Colon carcinoma HCT 116 cell CVCL_0291 [17]
Half Maximal Growth Inhibition (GI50) 2.65 nM Non-small cell lung carcinoma HOP-62 cell CVCL_1285 [18]
Half Maximal Growth Inhibition (GI50) 2.78 nM Melanoma M14 cell CVCL_1395 [18]
Half Maximal Growth Inhibition (GI50) 3 nM Plasma cell myeloma RPMI-8226 cell CVCL_7353 [15]
Half Maximal Growth Inhibition (GI50) 3 nM Cutaneous melanoma SK-MEL-5 cell CVCL_0527 [16]
Half Maximal Growth Inhibition (GI50) 3 nM Colon carcinoma HCT 116 cell CVCL_0291 [19]
Half Maximal Growth Inhibition (GI50) 3 nM Colon adenocarcinoma SW620 cell CVCL_0547 [19]
Half Maximal Growth Inhibition (GI50) 3.2 nM Lymphoma P388 cell CVCL_7222 [20]
Half Maximal Growth Inhibition (GI50) 4 nM Astrocytoma U-251MG cell CVCL_0021 [16]
Half Maximal Growth Inhibition (GI50) 4.55 nM Ovarian serous cystadenocarcinoma SK-OV-3 cell CVCL_0532 [21]
Half Maximal Growth Inhibition (GI50) 5 nM Melanoma UACC-62 cell CVCL_1780 [15]
Half Maximal Growth Inhibition (GI50) 5.51 nM Melanoma UACC-62 cell CVCL_1780 [18]
Half Maximal Growth Inhibition (GI50) 5.98 nM Renal cell carcinoma SN12C cell CVCL_1705 [18]
Half Maximal Growth Inhibition (GI50) 6 nM Renal cell carcinoma SN12C cell CVCL_1705 [15]
Half Maximal Growth Inhibition (GI50) 6 nM Renal carcinoma A498 cell CVCL_1056 [16]
Half Maximal Growth Inhibition (GI50) 6 nM Renal adenocarcinoma ACHN cell CVCL_1067 [19]
Half Maximal Growth Inhibition (GI50) 6 nM Melanoma UACC-62 cell CVCL_1780 [19]
Half Maximal Growth Inhibition (GI50) 6 nM Astrocytoma SF268 cell CVCL_1689 [19]
Half Maximal Growth Inhibition (GI50) 6 nM Astrocytoma U-251MG cell CVCL_0021 [14]
Half Maximal Growth Inhibition (GI50) 7 nM Minimally invasive lung adenocarcinoma NCI-H322M cell CVCL_1557 [19]
Half Maximal Growth Inhibition (GI50) 7 nM Lung squamous cell carcinoma NCI-H520 cell CVCL_1566 [14]
Half Maximal Growth Inhibition (GI50) 7 nM Glioblastoma SNB-75 cell CVCL_1706 [15]
Half Maximal Growth Inhibition (GI50) 8 nM Glioblastoma SNB-75 cell CVCL_1706 [19]
Half Maximal Growth Inhibition (GI50) 8 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [22]
Half Maximal Growth Inhibition (GI50) 10 nM Prostate carcinoma DU145 cell CVCL_0105 [23]
Half Maximal Growth Inhibition (GI50) 10 nM Melanoma UACC-62 cell CVCL_1780 [23]
Half Maximal Growth Inhibition (GI50) <10 nM Lung large cell carcinoma NCI-H460 cell CVCL_0459 [24]
Half Maximal Growth Inhibition (GI50) 10 nM Cutaneous melanoma SK-MEL-5 cell CVCL_0527 [23]
Half Maximal Growth Inhibition (GI50) <10 nM Colon adenocarcinoma HCT 15 cell CVCL_0292 [25]
Half Maximal Growth Inhibition (GI50) 10 nM Breast ductal carcinoma BT-549 cell CVCL_1092 [23]
Half Maximal Growth Inhibition (GI50) 10 nM Breast adenocarcinoma MDA-MB-231 cell CVCL_0062 [26]
Half Maximal Growth Inhibition (GI50) 15 nM Ovarian endometrioid adenocarcinoma IGROV-1 cell CVCL_1304 [19]
Half Maximal Growth Inhibition (GI50) 16 nM Lung adenocarcinoma A-549 cell CVCL_0023 [16]
Half Maximal Growth Inhibition (GI50) 18 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [16]
Half Maximal Growth Inhibition (GI50) 19 nM Renal carcinoma UO-31 cell CVCL_1911 [15]
Half Maximal Growth Inhibition (GI50) 19 nM Melanoma Malme-3M cell CVCL_1438 [15]
Half Maximal Growth Inhibition (GI50) 26 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [27]
Half Maximal Growth Inhibition (GI50) 31.6 nM Amelanotic melanoma MDA-MB-435 cell CVCL_0417 [28]
Half Maximal Growth Inhibition (GI50) 31.62 nM Prostate carcinoma PC-3 cell CVCL_0035 [29]
Half Maximal Growth Inhibition (GI50) 31.62 nM Lung large cell carcinoma NCI-H460 cell CVCL_0459 [23]
Half Maximal Growth Inhibition (GI50) 31.62 nM Colon carcinoma HCT 116 cell CVCL_0291 [23]
Half Maximal Growth Inhibition (GI50) 31.62 nM Colon adenocarcinoma HCT 15 cell CVCL_0292 [23]
Half Maximal Growth Inhibition (GI50) 31.62 nM Chronic myeloid leukemia K562 cell CVCL_0004 [23]
Half Maximal Growth Inhibition (GI50) 39.81 nM Prostate carcinoma PC-3 cell CVCL_0035 [23]
Half Maximal Growth Inhibition (GI50) 39.81 nM Ovarian serous adenocarcinoma OVCAR-3 cell CVCL_0465 [23]
Half Maximal Growth Inhibition (GI50) 39.81 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [23]
Half Maximal Growth Inhibition (GI50) 39.81 nM Clear cell renal cell carcinoma Caki-1 cell CVCL_0234 [23]
Half Maximal Growth Inhibition (GI50) 50.12 nM Colon adenocarcinoma KM12 cell CVCL_1331 [23]
Half Maximal Growth Inhibition (GI50) 63 nM Colon adenocarcinoma HCC 2998 cell CVCL_1266 [15]
Half Maximal Growth Inhibition (GI50) 63.1 nM High grade ovarian serous adenocarcinoma NCI-ADR-RES cell CVCL_1452 [23]
Half Maximal Growth Inhibition (GI50) 84 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [30]
Half Maximal Growth Inhibition (GI50) 84.1 nM Lung adenocarcinoma A-549 cell CVCL_0023 [31]
Half Maximal Growth Inhibition (GI50) 100 nM T acute lymphoblastic leukemia CCRF-CEM cell CVCL_0207 [29]
Half Maximal Growth Inhibition (GI50) 125.89 nM Astrocytoma SF268 cell CVCL_1689 [23]
Half Maximal Growth Inhibition (GI50) 158.49 nM Plasma cell myeloma RPMI-8226 cell CVCL_7353 [29]
Half Maximal Growth Inhibition (GI50) 199.53 nM Renal carcinoma UO-31 cell CVCL_1911 [23]
Half Maximal Growth Inhibition (GI50) 200 nM Colon cancer HT29 cell CVCL_A8EZ [1]
Half Maximal Growth Inhibition (GI50) 398.11 nM Non-small cell lung carcinoma EKVX cell CVCL_1195 [23]
Half Maximal Growth Inhibition (GI50) 630.96 nM Colon cancer HT29 cell CVCL_A8EZ [23]
Half Maximal Growth Inhibition (GI50) 631 nM Colon cancer HT29 cell CVCL_A8EZ [28]
Half Maximal Growth Inhibition (GI50) 794.33 nM Glioblastoma SNB-75 cell CVCL_1706 [23]
Half Maximal Growth Inhibition (GI50) 1000 nM Renal carcinoma RXF 393 cell CVCL_1673 [23]
Half Maximal Growth Inhibition (GI50) 2.51189 uM Normal COLO205 cell CVCL_F402 [23]
Half Maximal Growth Inhibition (GI50) 3.16228 uM Cutaneous melanoma SK-MEL-28 cell CVCL_0526 [23]
Half Maximal Growth Inhibition (GI50) 31.6 uM Ovarian serous cystadenocarcinoma SK-OV-3 cell CVCL_0532 [22]
Half Maximal Inhibitory Concentration (IC50) <1 ug/mL Endocervical adenocarcinoma L132 cell CVCL_1908 [32]
Half Maximal Inhibitory Concentration (IC50) 5 ug/mL Colon cancer HT29 cell CVCL_A8EZ [32]
Half Maximal Inhibitory Concentration (IC50) 57 ug/mL Prostate carcinoma DU145 cell CVCL_0105 [32]
Half Maximal Inhibitory Concentration (IC50) 28.2 pM Chronic myeloid leukemia K562 cell CVCL_0004 [33]
Half Maximal Inhibitory Concentration (IC50) 79.4 pM Colon carcinoma HCT 116 cell CVCL_0291 [33]
Half Maximal Inhibitory Concentration (IC50) 0.1 nM Acute myeloid leukemia HL-60 cell CVCL_0002 [34]
Half Maximal Inhibitory Concentration (IC50) 0.24 nM Invasive breast carcinoma ZR-75-1 cell CVCL_0588 [35]
Half Maximal Inhibitory Concentration (IC50) 0.8 nM T acute lymphoblastic leukemia Jurkat cell CVCL_0065 [36]
Half Maximal Inhibitory Concentration (IC50) 0.9 nM Colon carcinoma HCT 116 cell CVCL_0291 [37]
Half Maximal Inhibitory Concentration (IC50) 0.94 nM Lung adenocarcinoma Calu-6 cell CVCL_0236 [38]
Half Maximal Inhibitory Concentration (IC50) 1 nM Melanoma B16 cell CVCL_F936 [37]
Half Maximal Inhibitory Concentration (IC50) 1 nM Glioma A10 cell CVCL_0130 [39]
Half Maximal Inhibitory Concentration (IC50) 1 nM Colon carcinoma HCT 116 cell CVCL_0291 [40]
Half Maximal Inhibitory Concentration (IC50) 1 nM B acute lymphoblastic leukemia RS4
11 cell 		CVCL_0093 [41]
Half Maximal Inhibitory Concentration (IC50) 1.2 nM Lung large cell carcinoma NCI-H460 cell CVCL_0459 [42]
Half Maximal Inhibitory Concentration (IC50) 1.3 nM High grade ovarian serous adenocarcinoma OVCAR-8 cell CVCL_1629 [39]
Half Maximal Inhibitory Concentration (IC50) 1.4 nM Chronic myeloid leukemia K562 cell CVCL_0004 [43]
Half Maximal Inhibitory Concentration (IC50) 1.5 nM Bone marrow neuroblastoma SH-SY5Y cell CVCL_0019 [44]
Half Maximal Inhibitory Concentration (IC50) 1.52 nM Colon adenocarcinoma SW620 cell CVCL_0547 [45]
Half Maximal Inhibitory Concentration (IC50) 1.6 nM T acute lymphoblastic leukemia CCRF-CEM cell CVCL_0207 [46]
Half Maximal Inhibitory Concentration (IC50) 1.7 nM Colon adenocarcinoma HCT 15 cell CVCL_0292 [47]
Half Maximal Inhibitory Concentration (IC50) 1.9 nM T acute lymphoblastic leukemia CCRF-CEM cell CVCL_0207 [48]
Half Maximal Inhibitory Concentration (IC50) 1.9 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [49]
Half Maximal Inhibitory Concentration (IC50) 1.9 nM Acute myeloid leukemia HL-60 cell CVCL_0002 [50]
Half Maximal Inhibitory Concentration (IC50) 2 nM Melanoma B16 cell CVCL_F936 [51]
Half Maximal Inhibitory Concentration (IC50) 2 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [52]
Half Maximal Inhibitory Concentration (IC50) 2 nM Human papillomavirus-related endocervical adenocarcinoma KB cell CVCL_0372 [53]
Half Maximal Inhibitory Concentration (IC50) 2 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [54]
Half Maximal Inhibitory Concentration (IC50) 2 nM Acute myeloid leukemia HL-60 cell CVCL_0002 [55]
Half Maximal Inhibitory Concentration (IC50) 2.1 nM Human papillomavirus-related endocervical adenocarcinoma KB cell CVCL_0372 [56]
Half Maximal Inhibitory Concentration (IC50) 2.19 nM Ovarian endometrioid adenocarcinoma A2780 cell CVCL_0134 [52]
Half Maximal Inhibitory Concentration (IC50) 2.2 nM Colon carcinoma HCT 116 cell CVCL_0291 [57]
Half Maximal Inhibitory Concentration (IC50) 2.3 nM Colon carcinoma HCT 116 cell CVCL_0291 [58]
Half Maximal Inhibitory Concentration (IC50) 2.5 nM Lung small cell carcinoma H69AR cell CVCL_3513 [59]
Half Maximal Inhibitory Concentration (IC50) 2.5 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [60]
Half Maximal Inhibitory Concentration (IC50) 2.5 nM Human papillomavirus-related endocervical adenocarcinoma KB cell CVCL_0372 [61]
Half Maximal Inhibitory Concentration (IC50) 2.7 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [37]
Half Maximal Inhibitory Concentration (IC50) 2.7 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [59]
Half Maximal Inhibitory Concentration (IC50) 2.8 nM Prostate carcinoma PC-3 cell CVCL_0035 [62]
Half Maximal Inhibitory Concentration (IC50) 2.9 nM Colon adenocarcinoma LoVo cell CVCL_0399 [38]
Half Maximal Inhibitory Concentration (IC50) 3 nM Ovarian endometrioid adenocarcinoma A2780 cell CVCL_0134 [63]
Half Maximal Inhibitory Concentration (IC50) 3 nM Normal HBL-100 cell CVCL_4362 [64]
Half Maximal Inhibitory Concentration (IC50) 3 nM Lymphoblastic leukemia L1210 cell CVCL_0382 [65]
Half Maximal Inhibitory Concentration (IC50) 3 nM Lung large cell carcinoma NCI-H460 cell CVCL_0459 [66]
Half Maximal Inhibitory Concentration (IC50) 3 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [67]
Half Maximal Inhibitory Concentration (IC50) 3.1 nM Lymphoma P388 cell CVCL_7222 [43]
Half Maximal Inhibitory Concentration (IC50) 3.1 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [68]
Half Maximal Inhibitory Concentration (IC50) 3.162 nM Lymphoma P388 cell CVCL_7222 [69]
Half Maximal Inhibitory Concentration (IC50) 3.2 nM Colon adenocarcinoma HCT 15 cell CVCL_0292 [70]
Half Maximal Inhibitory Concentration (IC50) 3.3 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [71]
Half Maximal Inhibitory Concentration (IC50) 3.4 nM Amelanotic melanoma MDA-MB-435 cell CVCL_0417 [72]
Half Maximal Inhibitory Concentration (IC50) 3.5 nM High grade ovarian serous adenocarcinoma NCI-ADR-RES cell CVCL_1452 [73]
Half Maximal Inhibitory Concentration (IC50) 3.5 nM Breast ductal carcinoma BT-549 cell CVCL_1092 [38]
Half Maximal Inhibitory Concentration (IC50) 3.6 nM Chronic myeloid leukemia K562 cell CVCL_0004 [58]
Half Maximal Inhibitory Concentration (IC50) 3.8 nM Lung adenocarcinoma A-549 cell CVCL_0023 [74]
Half Maximal Inhibitory Concentration (IC50) 3.8 nM Hepatocellular carcinoma SMMC-7721 cell CVCL_0534 [75]
Half Maximal Inhibitory Concentration (IC50) 3.9 nM Hepatoblastoma Hep-G2 cell CVCL_0027 [76]
Half Maximal Inhibitory Concentration (IC50) 4 nM Lung adenocarcinoma A-549 cell CVCL_0023 [63]
Half Maximal Inhibitory Concentration (IC50) 4 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [77]
Half Maximal Inhibitory Concentration (IC50) 4 nM High grade ovarian serous adenocarcinoma OVCAR-8 cell CVCL_1629 [73]
Half Maximal Inhibitory Concentration (IC50) 4 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [41]
Half Maximal Inhibitory Concentration (IC50) 4 nM Colon carcinoma HCT 116 cell CVCL_0291 [78]
Half Maximal Inhibitory Concentration (IC50) 4 nM Breast adenocarcinoma MDA-MB-231 cell CVCL_0062 [79]
Half Maximal Inhibitory Concentration (IC50) 4.09 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [80]
Half Maximal Inhibitory Concentration (IC50) 4.1 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [81]
Half Maximal Inhibitory Concentration (IC50) 4.3 nM Melanoma M21 cell CVCL_D031 [82]
Half Maximal Inhibitory Concentration (IC50) 4.5 nM Ovarian serous cystadenocarcinoma SK-OV-3 cell CVCL_0532 [83]
Half Maximal Inhibitory Concentration (IC50) 4.7 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [84]
Half Maximal Inhibitory Concentration (IC50) 5 nM T acute lymphoblastic leukemia Jurkat cell CVCL_0065 [85]
Half Maximal Inhibitory Concentration (IC50) 5 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [86]
Half Maximal Inhibitory Concentration (IC50) 5 nM Amelanotic melanoma MDA-MB-435 cell CVCL_0417 [87]
Half Maximal Inhibitory Concentration (IC50) 5.1 nM Colon cancer HT29 cell CVCL_A8EZ [88]
Half Maximal Inhibitory Concentration (IC50) 5.5 nM Ovarian serous cystadenocarcinoma SK-OV-3 cell CVCL_0532 [38]
Half Maximal Inhibitory Concentration (IC50) 5.6 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [82]
Half Maximal Inhibitory Concentration (IC50) 5.6 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [87]
Half Maximal Inhibitory Concentration (IC50) 5.7 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [83]
Half Maximal Inhibitory Concentration (IC50) 6 nM Ovarian endometrioid adenocarcinoma A2780 cell CVCL_0134 [89]
Half Maximal Inhibitory Concentration (IC50) 6 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [90]
Half Maximal Inhibitory Concentration (IC50) 6 nM Hepatocellular carcinoma SNU-423 cell CVCL_0366 [79]
Half Maximal Inhibitory Concentration (IC50) 6 nM Chronic myeloid leukemia K562 cell CVCL_0004 [91]
Half Maximal Inhibitory Concentration (IC50) 6.05 nM Ovarian serous cystadenocarcinoma SK-OV-3 cell CVCL_0532 [80]
Half Maximal Inhibitory Concentration (IC50) 7 nM Human papillomavirus-related endocervical adenocarcinoma KB cell CVCL_0372 [92]
Half Maximal Inhibitory Concentration (IC50) 7 nM Colon carcinoma HCT 116 cell CVCL_0291 [76]
Half Maximal Inhibitory Concentration (IC50) 7 nM Chronic myeloid leukemia K562 cell CVCL_0004 [93]
Half Maximal Inhibitory Concentration (IC50) 7.2 nM Ovarian serous cystadenocarcinoma SK-OV-3 cell CVCL_0532 [94]
Half Maximal Inhibitory Concentration (IC50) 8 nM Pancreatic ductal adenocarcinoma MIA PaCa-2 cell CVCL_0428 [79]
Half Maximal Inhibitory Concentration (IC50) 8 nM Human papillomavirus-related endocervical adenocarcinoma KB cell CVCL_0372 [95]
Half Maximal Inhibitory Concentration (IC50) 8 nM Breast adenocarcinoma MDA-MB-231 cell CVCL_0062 [96]
Half Maximal Inhibitory Concentration (IC50) 9 nM Lung adenocarcinoma A-549 cell CVCL_0023 [93]
Half Maximal Inhibitory Concentration (IC50) 9.3 nM T-lymphoblastic leukemia MOLT-3 cell CVCL_0624 [48]
Half Maximal Inhibitory Concentration (IC50) 9.3 nM Prostate carcinoma DU145 cell CVCL_0105 [62]
Half Maximal Inhibitory Concentration (IC50) 9.5 nM Human papillomavirus-related endocervical adenocarcinoma KB cell CVCL_0372 [92]
Half Maximal Inhibitory Concentration (IC50) 9.7 nM Ovarian serous cystadenocarcinoma SK-OV-3 cell CVCL_0532 [97]
Half Maximal Inhibitory Concentration (IC50) 9.8 nM Colon carcinoma RKO cell CVCL_0504 [76]
Half Maximal Inhibitory Concentration (IC50) 10 nM Lung adenocarcinoma A-549 cell CVCL_0023 [98]
Half Maximal Inhibitory Concentration (IC50) 10 nM Hepatoma Bel-7402 cell CVCL_5492 [62]
Half Maximal Inhibitory Concentration (IC50) 10 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [96]
Half Maximal Inhibitory Concentration (IC50) 11 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [99]
Half Maximal Inhibitory Concentration (IC50) 11 nM Hepatoma Bel-7402 cell CVCL_5492 [100]
Half Maximal Inhibitory Concentration (IC50) 12 nM Ovarian endometrioid adenocarcinoma A2780 cell CVCL_0134 [76]
Half Maximal Inhibitory Concentration (IC50) 12 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [62]
Half Maximal Inhibitory Concentration (IC50) 12 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [101]
Half Maximal Inhibitory Concentration (IC50) 13 nM Uterine sarcoma MES-SA cell CVCL_1404 [102]
Half Maximal Inhibitory Concentration (IC50) 13 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [103]
Half Maximal Inhibitory Concentration (IC50) 13 nM Acute myeloid leukemia HL-60 cell CVCL_0002 [104]
Half Maximal Inhibitory Concentration (IC50) 14 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [76]
Half Maximal Inhibitory Concentration (IC50) 14.2 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [105]
Half Maximal Inhibitory Concentration (IC50) 15 nM Ileocecal adenocarcinoma HCT-8 cell CVCL_2478 [106]
Half Maximal Inhibitory Concentration (IC50) 20 nM Chronic myeloid leukemia K562 cell CVCL_0004 [107]
Half Maximal Inhibitory Concentration (IC50) 20 nM Burkitt lymphoma CA46 cell CVCL_1101 [108]
Half Maximal Inhibitory Concentration (IC50) 21.6 nM Bladder carcinoma RT-112 cell CVCL_1670 [54]
Half Maximal Inhibitory Concentration (IC50) 22 nM Ovarian serous cystadenocarcinoma SK-OV-3 cell CVCL_0532 [81]
Half Maximal Inhibitory Concentration (IC50) 23.43 nM Colon adenocarcinoma T84 cell CVCL_0555 [45]
Half Maximal Inhibitory Concentration (IC50) 25 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [109]
Half Maximal Inhibitory Concentration (IC50) 29 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [46]
Half Maximal Inhibitory Concentration (IC50) 32 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [110]
Half Maximal Inhibitory Concentration (IC50) 32 nM Colon cancer HT29 cell CVCL_A8EZ [55]
Half Maximal Inhibitory Concentration (IC50) 37 nM Lung adenocarcinoma A-549 cell CVCL_0023 [111]
Half Maximal Inhibitory Concentration (IC50) 41 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [112]
Half Maximal Inhibitory Concentration (IC50) 42 nM Malignant neoplasms of the mouse mammary gland FM3A cell CVCL_3869 [65]
Half Maximal Inhibitory Concentration (IC50) 42 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [113]
Half Maximal Inhibitory Concentration (IC50) 46 nM Chronic myeloid leukemia K562 cell CVCL_0004 [114]
Half Maximal Inhibitory Concentration (IC50) <50 nM Pancreatic ductal adenocarcinoma BxPC-3 cell CVCL_0186 [95]
Half Maximal Inhibitory Concentration (IC50) 50 nM Mouse melanoma B16-F10 cell CVCL_0159 [115]
Half Maximal Inhibitory Concentration (IC50) 52 nM Breast carcinoma MX1 cell CVCL_4774 [95]
Half Maximal Inhibitory Concentration (IC50) 71 nM Breast carcinoma MX1 cell CVCL_4774 [95]
Half Maximal Inhibitory Concentration (IC50) 80 nM Lung large cell carcinoma NCI-H460 cell CVCL_0459 [116]
Half Maximal Inhibitory Concentration (IC50) 82 nM Gastric adenocarcinoma MKN45 cell CVCL_0434 [102]
Half Maximal Inhibitory Concentration (IC50) 87.2 nM Colon cancer HT29 cell CVCL_A8EZ [61]
Half Maximal Inhibitory Concentration (IC50) 94 nM Colon cancer HT29 cell CVCL_A8EZ [53]
Half Maximal Inhibitory Concentration (IC50) 94.3 nM Lung adenocarcinoma A-549 cell CVCL_0023 [105]
Half Maximal Inhibitory Concentration (IC50) 120 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [117]
Half Maximal Inhibitory Concentration (IC50) 124 nM Small cell lung carcinoma DMS-79 cell CVCL_1178 [62]
Half Maximal Inhibitory Concentration (IC50) 160 nM Pancreatic ductal adenocarcinoma PANC-1 cell CVCL_0480 [118]
Half Maximal Inhibitory Concentration (IC50) 160 nM Lymphoma P388 cell CVCL_7222 [119]
Half Maximal Inhibitory Concentration (IC50) 160 nM Lung adenocarcinoma A-549 cell CVCL_0023 [120]
Half Maximal Inhibitory Concentration (IC50) 170 nM Renal adenocarcinoma ACHN cell CVCL_1067 [121]
Half Maximal Inhibitory Concentration (IC50) 180 nM Lung adenocarcinoma A-549 cell CVCL_0023 [122]
Half Maximal Inhibitory Concentration (IC50) 180 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [121]
Half Maximal Inhibitory Concentration (IC50) 190 nM Normal HaCaT cell CVCL_0038 [123]
Half Maximal Inhibitory Concentration (IC50) 190 nM Hepatoblastoma Hep-G2 cell CVCL_0027 [124]
Half Maximal Inhibitory Concentration (IC50) 200 nM Lung adenocarcinoma A-549 cell CVCL_0023 [33]
Half Maximal Inhibitory Concentration (IC50) 210 nM Amelanotic melanoma A-375 cell CVCL_0132 [121]
Half Maximal Inhibitory Concentration (IC50) 240 nM Endocervical adenocarcinoma HeLa cell CVCL_0030 [120]
Half Maximal Inhibitory Concentration (IC50) 250 nM Pancreatic adenocarcinoma SW1990 cell CVCL_1723 [46]
Half Maximal Inhibitory Concentration (IC50) 260 nM Colon cancer HT29 cell CVCL_A8EZ [56]
Half Maximal Inhibitory Concentration (IC50) 280 nM Prostate carcinoma DU145 cell CVCL_0105 [125]
Half Maximal Inhibitory Concentration (IC50) 330 nM Hepatoblastoma Hep-G2 cell CVCL_0027 [120]
Half Maximal Inhibitory Concentration (IC50) 370 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [126]
Half Maximal Inhibitory Concentration (IC50) 400 nM Prostate carcinoma PC-3 cell CVCL_0035 [39]
Half Maximal Inhibitory Concentration (IC50) 410 nM Invasive breast carcinoma MCF-7 cell CVCL_0031 [127]
Half Maximal Inhibitory Concentration (IC50) 420 nM Lung adenocarcinoma A-549 cell CVCL_0023 [114]
Half Maximal Inhibitory Concentration (IC50) 430 nM Hepatocellular carcinoma Huh-7 cell CVCL_0336 [109]
Half Maximal Inhibitory Concentration (IC50) 540 nM Astrocytoma U-251MG cell CVCL_0021 [128]
Half Maximal Inhibitory Concentration (IC50) 560 nM Acute myeloid leukemia HL-60 cell CVCL_0002 [129]
Half Maximal Inhibitory Concentration (IC50) 720 nM Colon cancer HT29 cell CVCL_A8EZ [130]
Half Maximal Inhibitory Concentration (IC50) >1000 nM Colon cancer HT29 cell CVCL_A8EZ [59]
Half Maximal Inhibitory Concentration (IC50) 1000 nM Colon cancer HT29 cell CVCL_A8EZ [90]
Half Maximal Inhibitory Concentration (IC50) 1000 nM Chronic myeloid leukemia K562 cell CVCL_0004 [131]
Half Maximal Inhibitory Concentration (IC50) 1.3 uM High grade ovarian serous adenocarcinoma OVCAR-8 cell CVCL_1629 [132]
Half Maximal Inhibitory Concentration (IC50) 1.718 uM Hepatoma Bel-7402 cell CVCL_5492 [46]
Half Maximal Inhibitory Concentration (IC50) 1.8 uM Endocervical adenocarcinoma HeLa cell CVCL_0030 [132]
Half Maximal Inhibitory Concentration (IC50) 2.41 uM Hepatoblastoma Hep-G2 cell CVCL_0027 [129]
Half Maximal Inhibitory Concentration (IC50) 2.5 uM Endocervical adenocarcinoma HeLa cell CVCL_0030 [132]
Half Maximal Inhibitory Concentration (IC50) 3.1 uM Colon cancer HT29 cell CVCL_A8EZ [122]
Half Maximal Inhibitory Concentration (IC50) 3.2 uM Chronic myeloid leukemia K562 cell CVCL_0004 [43]
Half Maximal Inhibitory Concentration (IC50) 3.22 uM Hepatocellular carcinoma SMMC-7721 cell CVCL_0534 [114]
Half Maximal Inhibitory Concentration (IC50) 3.27 uM Cervical carcinoma L02 cell CVCL_6926 [133]
Half Maximal Inhibitory Concentration (IC50) 3.4 uM Normal HMEC-1 cell CVCL_0307 [134]
Half Maximal Inhibitory Concentration (IC50) 3.6 uM Colon cancer HT29 cell CVCL_A8EZ [34]
Half Maximal Inhibitory Concentration (IC50) 4 uM Acute myeloid leukemia HL-60 cell CVCL_0002 [134]
Half Maximal Inhibitory Concentration (IC50) 4.165 uM Colon cancer HT29 cell CVCL_A8EZ [77]
Half Maximal Inhibitory Concentration (IC50) 5.99 uM Lung adenocarcinoma A-549 cell CVCL_0023 [135]
Half Maximal Inhibitory Concentration (IC50) 6.1 uM Colon carcinoma HCT 116 cell CVCL_0291 [136]
Half Maximal Inhibitory Concentration (IC50) 8.87 uM Colon adenocarcinoma HCT 15 cell CVCL_0292 [125]
Half Maximal Inhibitory Concentration (IC50) 9.12 uM Colon carcinoma HCT 116 cell CVCL_0291 [125]
Half Maximal Inhibitory Concentration (IC50) >10 uM Lung adenocarcinoma A-549 cell CVCL_0023 [39]
Half Maximal Inhibitory Concentration (IC50) >10 uM Gastric carcinoma NUGC-3 cell CVCL_1612 [102]
Half Maximal Inhibitory Concentration (IC50) >10 uM Colon cancer HT29 cell CVCL_A8EZ [39]
Half Maximal Inhibitory Concentration (IC50) 11 uM Normal HEK293 cell CVCL_0045 [115]
Half Maximal Inhibitory Concentration (IC50) >20 uM Lung adenocarcinoma A-549 cell CVCL_0023 [123]
Half Maximal Inhibitory Concentration (IC50) 25 uM Normal HEK293 cell CVCL_0045 [134]
Tumor Growth Inhibition value (TGI) 79.43 nM Amelanotic melanoma MDA-MB-435 cell CVCL_0417 [23]
Tumor Growth Inhibition value (TGI) 158.49 nM Ovarian serous adenocarcinoma OVCAR-3 cell CVCL_0465 [23]
Tumor Growth Inhibition value (TGI) 199.53 nM Colon carcinoma HCT 116 cell CVCL_0291 [23]
Tumor Growth Inhibition value (TGI) 251.19 nM Melanoma M14 cell CVCL_1395 [23]
Tumor Growth Inhibition value (TGI) 794.33 nM Colon adenocarcinoma KM12 cell CVCL_1331 [23]
Tumor Growth Inhibition value (TGI) 1.25893 uM Glioblastoma SF-295 cell CVCL_1690 [23]
Tumor Growth Inhibition value (TGI) 1.25893 uM Colon adenocarcinoma HCC 2998 cell CVCL_1266 [23]
Tumor Growth Inhibition value (TGI) 1.99526 uM Chronic myeloid leukemia K562 cell CVCL_0004 [23]
Tumor Growth Inhibition value (TGI) 1.99526 uM Breast ductal carcinoma BT-549 cell CVCL_1092 [23]
Tumor Growth Inhibition value (TGI) 2.51189 uM Non-small cell lung carcinoma HOP-62 cell CVCL_1285 [23]
Tumor Growth Inhibition value (TGI) 3.98107 uM T acute lymphoblastic leukemia MOLT-4 cell CVCL_0013 [23]
Tumor Growth Inhibition value (TGI) 3.98107 uM Non-small cell lung carcinoma NCI-H522 cell CVCL_1567 [23]
Tumor Growth Inhibition value (TGI) 5.01187 uM T acute lymphoblastic leukemia CCRF-CEM cell CVCL_0207 [23]
Tumor Growth Inhibition value (TGI) 6.30957 uM Colon cancer HT29 cell CVCL_A8EZ [23]
Tumor Growth Inhibition value (TGI) 12.58925 uM Astrocytoma U-251MG cell CVCL_0021 [23]
Tumor Growth Inhibition value (TGI) 39.81072 uM High grade ovarian serous adenocarcinoma OVCAR-8 cell CVCL_1629 [23]
Tumor Growth Inhibition value (TGI) 50.11872 uM Renal carcinoma UO-31 cell CVCL_1911 [23]
Tumor Growth Inhibition value (TGI) 50.11872 uM Cutaneous melanoma SK-MEL-28 cell CVCL_0526 [23]
Tumor Growth Inhibition value (TGI) 63.09573 uM Ovarian endometrioid adenocarcinoma IGROV-1 cell CVCL_1304 [23]
Tumor Growth Inhibition value (TGI) 63.09573 uM Melanoma UACC-62 cell CVCL_1780 [23]
Tumor Growth Inhibition value (TGI) 79.43282 uM Renal carcinoma RXF 393 cell CVCL_1673 [23]
Tumor Growth Inhibition value (TGI) 79.43282 uM Non-small cell lung carcinoma EKVX cell CVCL_1195 [23]
Tumor Growth Inhibition value (TGI) 79.43282 uM Minimally invasive lung adenocarcinoma NCI-H322M cell CVCL_1557 [23]
Tumor Growth Inhibition value (TGI) 79.43282 uM Melanoma Malme-3M cell CVCL_1438 [23]
Tumor Growth Inhibition value (TGI) 79.43282 uM Leukemia SR cell CVCL_1711 [23]
Tumor Growth Inhibition value (TGI) 79.43282 uM Colon adenocarcinoma SW620 cell CVCL_0547 [23]
Tumor Growth Inhibition value (TGI) 100 uM Prostate carcinoma DU145 cell CVCL_0105 [23]
Tumor Growth Inhibition value (TGI) 100 uM Prostate carcinoma PC-3 cell CVCL_0035 [23]
Tumor Growth Inhibition value (TGI) 100 uM Ovarian serous cystadenocarcinoma SK-OV-3 cell CVCL_0532 [23]
Tumor Growth Inhibition value (TGI) 100 uM Invasive breast carcinoma T-47D cell CVCL_0553 [23]
Each Peptide-drug Conjugate Related to This Drug
Full Information of The Activity Data of The PDC(s) Related to This Drug
NT4-CA4 ester [Investigative]
 PDC Info 
Revealed Based on the Cell Line Data
Click To Hide/Show 3 Activity Data Related to This Level
Experiment 1 Reporting the Activity Data of This PDC [137]
Indication Solid tumor
Efficacy Data Cell viability 0.00%
Administration Time 6 days
Administration Dosage 0.03 mM
MOA of PDC
We have been studying protease-resistant branched peptides as tumor targeting agents by using tetra-branched peptides (NT4) containing the human regulatory peptide neurotensin (NT) sequence. Neurotensin receptors are overexpressed in several human malignancies, such as colon, pancreatic, prostate and small-cell lung cancer. We have been using NT4 conjugated to different functional units for tumor imaging and therapy, and found that NT4 conjugated to methotrexate produced 60% reduction of tumor growth in xenografted mice. Results obtained with NT4 indicated that branched peptides are promising novel multifunctional targeting molecules, which might allow cancer detection and therapy by means of the same molecule, with no modification in target binding, but rather a simple exchange of functional units. Since cancer cells are very different from one another in terms of drug sensibility, not only in different tumors but in different patients and stages of the disease, this approach prefigures the synthesis of a number of constructs conjugated with differently acting chemotherapeutics. The type of linkage between effector unit (drug/imaging agent etc.) and peptide is obviously crucial for this type of approach. The choice must be driven by two issues: 1) The nature of the drug functional groups available for coupling with the peptide; and 2) the mechanism-of-action of the drug. When a prodrug acts without being released from the carrier unit, a strong linker is preferred. However, if a drug has to be released in order to interact with the intracellular target, the linker must be cleavable. In latter, the linker has to be chosen properly-not too labile or leakage will occur during drug distribution, but not too robust or the pharmacological action will be impaired.

   Click to Show/Hide
Description
This clearly indicated that the chemotherapeutic moiety was released into the cell medium and the drug was internalized into the cells, probably by membrane diffusion. This became evident when observing the behavior of the unrelated conjugated peptides.
In Vitro Model Pancreatic ductal adenocarcinoma PANC-1 cell CVCL_0480
Experiment 2 Reporting the Activity Data of This PDC [137]
Indication Solid tumor
Efficacy Data Cell viability 20.00%
Administration Time 6 days
Administration Dosage 0.03 mM
MOA of PDC
We have been studying protease-resistant branched peptides as tumor targeting agents by using tetra-branched peptides (NT4) containing the human regulatory peptide neurotensin (NT) sequence. Neurotensin receptors are overexpressed in several human malignancies, such as colon, pancreatic, prostate and small-cell lung cancer. We have been using NT4 conjugated to different functional units for tumor imaging and therapy, and found that NT4 conjugated to methotrexate produced 60% reduction of tumor growth in xenografted mice. Results obtained with NT4 indicated that branched peptides are promising novel multifunctional targeting molecules, which might allow cancer detection and therapy by means of the same molecule, with no modification in target binding, but rather a simple exchange of functional units. Since cancer cells are very different from one another in terms of drug sensibility, not only in different tumors but in different patients and stages of the disease, this approach prefigures the synthesis of a number of constructs conjugated with differently acting chemotherapeutics. The type of linkage between effector unit (drug/imaging agent etc.) and peptide is obviously crucial for this type of approach. The choice must be driven by two issues: 1) The nature of the drug functional groups available for coupling with the peptide; and 2) the mechanism-of-action of the drug. When a prodrug acts without being released from the carrier unit, a strong linker is preferred. However, if a drug has to be released in order to interact with the intracellular target, the linker must be cleavable. In latter, the linker has to be chosen properly-not too labile or leakage will occur during drug distribution, but not too robust or the pharmacological action will be impaired.

   Click to Show/Hide
Description
This clearly indicated that the chemotherapeutic moiety was released into the cell medium and the drug was internalized into the cells, probably by membrane diffusion. This became evident when observing the behavior of the unrelated conjugated peptides.
In Vitro Model Prostate carcinoma PC-3 cell CVCL_0035
Experiment 3 Reporting the Activity Data of This PDC [137]
Indication Solid tumor
Efficacy Data Cell viability 100.00%
Administration Time 6 days
Administration Dosage 0.03 mM
MOA of PDC
We have been studying protease-resistant branched peptides as tumor targeting agents by using tetra-branched peptides (NT4) containing the human regulatory peptide neurotensin (NT) sequence. Neurotensin receptors are overexpressed in several human malignancies, such as colon, pancreatic, prostate and small-cell lung cancer. We have been using NT4 conjugated to different functional units for tumor imaging and therapy, and found that NT4 conjugated to methotrexate produced 60% reduction of tumor growth in xenografted mice. Results obtained with NT4 indicated that branched peptides are promising novel multifunctional targeting molecules, which might allow cancer detection and therapy by means of the same molecule, with no modification in target binding, but rather a simple exchange of functional units. Since cancer cells are very different from one another in terms of drug sensibility, not only in different tumors but in different patients and stages of the disease, this approach prefigures the synthesis of a number of constructs conjugated with differently acting chemotherapeutics. The type of linkage between effector unit (drug/imaging agent etc.) and peptide is obviously crucial for this type of approach. The choice must be driven by two issues: 1) The nature of the drug functional groups available for coupling with the peptide; and 2) the mechanism-of-action of the drug. When a prodrug acts without being released from the carrier unit, a strong linker is preferred. However, if a drug has to be released in order to interact with the intracellular target, the linker must be cleavable. In latter, the linker has to be chosen properly-not too labile or leakage will occur during drug distribution, but not too robust or the pharmacological action will be impaired.

   Click to Show/Hide
Description
This clearly indicated that the chemotherapeutic moiety was released into the cell medium and the drug was internalized into the cells, probably by membrane diffusion. This became evident when observing the behavior of the unrelated conjugated peptides.
In Vitro Model Colon adenocarcinoma HT-29 cell CVCL_0320
NT4-CA4 ether [Investigative]
 PDC Info 
Revealed Based on the Cell Line Data
Click To Hide/Show 3 Activity Data Related to This Level
Experiment 1 Reporting the Activity Data of This PDC [137]
Indication Solid tumor
Efficacy Data Cell viability 0.00%
Administration Time 6 days
Administration Dosage 0.03 mM
MOA of PDC
We have been studying protease-resistant branched peptides as tumor targeting agents by using tetra-branched peptides (NT4) containing the human regulatory peptide neurotensin (NT) sequence. Neurotensin receptors are overexpressed in several human malignancies, such as colon, pancreatic, prostate and small-cell lung cancer. We have been using NT4 conjugated to different functional units for tumor imaging and therapy, and found that NT4 conjugated to methotrexate produced 60% reduction of tumor growth in xenografted mice. Results obtained with NT4 indicated that branched peptides are promising novel multifunctional targeting molecules, which might allow cancer detection and therapy by means of the same molecule, with no modification in target binding, but rather a simple exchange of functional units. Since cancer cells are very different from one another in terms of drug sensibility, not only in different tumors but in different patients and stages of the disease, this approach prefigures the synthesis of a number of constructs conjugated with differently acting chemotherapeutics. The type of linkage between effector unit (drug/imaging agent etc.) and peptide is obviously crucial for this type of approach. The choice must be driven by two issues: 1) The nature of the drug functional groups available for coupling with the peptide; and 2) the mechanism-of-action of the drug. When a prodrug acts without being released from the carrier unit, a strong linker is preferred. However, if a drug has to be released in order to interact with the intracellular target, the linker must be cleavable. In latter, the linker has to be chosen properly-not too labile or leakage will occur during drug distribution, but not too robust or the pharmacological action will be impaired.

   Click to Show/Hide
Description
This clearly indicated that the chemotherapeutic moiety was released into the cell medium and the drug was internalized into the cells, probably by membrane diffusion. This became evident when observing the behavior of the unrelated conjugated peptides.
In Vitro Model Colon adenocarcinoma HT-29 cell CVCL_0320
Experiment 2 Reporting the Activity Data of This PDC [137]
Indication Solid tumor
Efficacy Data Cell viability 0.00%
Administration Time 6 days
Administration Dosage 0.03 mM
MOA of PDC
We have been studying protease-resistant branched peptides as tumor targeting agents by using tetra-branched peptides (NT4) containing the human regulatory peptide neurotensin (NT) sequence. Neurotensin receptors are overexpressed in several human malignancies, such as colon, pancreatic, prostate and small-cell lung cancer. We have been using NT4 conjugated to different functional units for tumor imaging and therapy, and found that NT4 conjugated to methotrexate produced 60% reduction of tumor growth in xenografted mice. Results obtained with NT4 indicated that branched peptides are promising novel multifunctional targeting molecules, which might allow cancer detection and therapy by means of the same molecule, with no modification in target binding, but rather a simple exchange of functional units. Since cancer cells are very different from one another in terms of drug sensibility, not only in different tumors but in different patients and stages of the disease, this approach prefigures the synthesis of a number of constructs conjugated with differently acting chemotherapeutics. The type of linkage between effector unit (drug/imaging agent etc.) and peptide is obviously crucial for this type of approach. The choice must be driven by two issues: 1) The nature of the drug functional groups available for coupling with the peptide; and 2) the mechanism-of-action of the drug. When a prodrug acts without being released from the carrier unit, a strong linker is preferred. However, if a drug has to be released in order to interact with the intracellular target, the linker must be cleavable. In latter, the linker has to be chosen properly-not too labile or leakage will occur during drug distribution, but not too robust or the pharmacological action will be impaired.

   Click to Show/Hide
Description
This clearly indicated that the chemotherapeutic moiety was released into the cell medium and the drug was internalized into the cells, probably by membrane diffusion. This became evident when observing the behavior of the unrelated conjugated peptides.
In Vitro Model Prostate carcinoma PC-3 cell CVCL_0035
Experiment 3 Reporting the Activity Data of This PDC [137]
Indication Solid tumor
Efficacy Data Cell viability 55.00%
Administration Time 6 days
Administration Dosage 0.03 mM
MOA of PDC
We have been studying protease-resistant branched peptides as tumor targeting agents by using tetra-branched peptides (NT4) containing the human regulatory peptide neurotensin (NT) sequence. Neurotensin receptors are overexpressed in several human malignancies, such as colon, pancreatic, prostate and small-cell lung cancer. We have been using NT4 conjugated to different functional units for tumor imaging and therapy, and found that NT4 conjugated to methotrexate produced 60% reduction of tumor growth in xenografted mice. Results obtained with NT4 indicated that branched peptides are promising novel multifunctional targeting molecules, which might allow cancer detection and therapy by means of the same molecule, with no modification in target binding, but rather a simple exchange of functional units. Since cancer cells are very different from one another in terms of drug sensibility, not only in different tumors but in different patients and stages of the disease, this approach prefigures the synthesis of a number of constructs conjugated with differently acting chemotherapeutics. The type of linkage between effector unit (drug/imaging agent etc.) and peptide is obviously crucial for this type of approach. The choice must be driven by two issues: 1) The nature of the drug functional groups available for coupling with the peptide; and 2) the mechanism-of-action of the drug. When a prodrug acts without being released from the carrier unit, a strong linker is preferred. However, if a drug has to be released in order to interact with the intracellular target, the linker must be cleavable. In latter, the linker has to be chosen properly-not too labile or leakage will occur during drug distribution, but not too robust or the pharmacological action will be impaired.

   Click to Show/Hide
Description
This clearly indicated that the chemotherapeutic moiety was released into the cell medium and the drug was internalized into the cells, probably by membrane diffusion. This became evident when observing the behavior of the unrelated conjugated peptides.
In Vitro Model Pancreatic ductal adenocarcinoma PANC-1 cell CVCL_0480
References
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