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Target Identification Data Package

This package has 10 modules. The Drugs Module has 19 tables. Preview the first five rows of each table or Explore the schema

Drugs Module

19 Tables

This module provides a comprehensive list of all approved and investigational drugs. Each drug includes detailed molecular descriptions and relevant nomenclature and identifiers. The dataset includes coverage of small molecule drugs and biologics.

Accession Numbers

Numbers are assigned to drugs, categories, and conditions in order to identify the record.

id
number
record_id
record_type
primary
0
DB00001
1
Drug
1
1
BIOD00024
1
Drug
0
2
BTD00024
1
Drug
0
3
DB00002
2
Drug
1
4
BIOD00071
2
Drug
0
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Affected Organisms

Organisms in which the drug may display activity; activity may depend on local susceptibility patterns and resistance.

organism_id
drug_id
1
1
1
2
1
3
1
4
1
5
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Brands

The proprietary names used by the manufacturers for commercially available forms of the drug, focusing on brand names for products that are available in countries other than Canada and the United States.

id
drug_id
name
company
score
source
16
11
Wellferon
GlaxoSmithKline
good
23
16
Epogin
Chugai
good
33
20
Leucomax
Novartis
good
35
9559
Secremax
Repligen Corp
good
36
22
PEG-Intron
Schering Corp
good
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Drug Availabilities

Drug availability information is stored in the drug_availabilities table. Each row denotes the availability of a drug in a region.

drug_id
region
max_phase
marketed_prescription
marketed_prescription_started_on
marketed_prescription_ended_on
generic_available
generic_available_on
mixture_available
mixture_available_on
marketed_otc
marketed_otc_started_on
marketed_otc_ended_on
marketed_unapproved
marketed_unapproved_started_on
marketed_unapproved_ended_on
pre_market_cancelled
pre_market_cancelled_on
post_market_cancelled
post_market_cancelled_on
1
at
0
0
0
0
0
0
0
0
1
ca
4
1
2000-01-31
2013-07-26
0
0
0
0
0
1
2013-07-26
1
co
0
0
0
0
0
0
0
0
1
eu
4
1
2016-09-08
2012-07-27
0
0
0
0
1
0
1
idn
0
0
0
0
0
0
0
0
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Drug Calculated Properties

Drug properties that have been predicted by ChemAxon or ALOGPS based on the inputed chemical structure. Associated links below will redirect to descriptions of the specific term.

drug_id
iupac_name
iupac_traditional_name
smiles
logp
average_mass
mono_mass
formula
inchi
inchikey
polar_surface_area
refractivity
polarizability
rotatable_bond_count
acceptor_count
donor_count
pka_strongest_acidic
pka_strongest_basic
physiological_charge
number_of_rings
bioavailability
rule_of_five
ghose_filter
veber_rule
mddr_like_rule
alogps_logp
alogps_logs
alogps_solubility
6
(4S)-4-[(2S)-2-[(2S)-2-[(2S)-2-{2-[(2S)-2-(2-{2-[2-(2-{[(2S)-1-[(2S)-2-{[(2S)-1-[(2R)-2-amino-3-phenylpropanoyl]pyrrolidin-2-yl]formamido}-5-carbamimidamidopentanoyl]pyrrolidin-2-yl]formamido}acetamido)acetamido]acetamido}acetamido)-3-carbamoylpropanamido]acetamido}-3-carboxypropanamido]-3-phenylpropanamido]-4-carboxybutanamido]-4-{[(2S,3S)-1-[(2S)-2-{[(1S)-3-carboxy-1-{[(1S)-3-carboxy-1-{[(1S)-1-{[(1S)-1-carboxy-3-methylbutyl]carbamoyl}-2-(4-hydroxyphenyl)ethyl]carbamoyl}propyl]carbamoyl}propyl]carbamoyl}pyrrolidin-1-yl]-3-methyl-1-oxopentan-2-yl]carbamoyl}butanoic acid
bivalirudin
CC[C@H](C)[C@H](NC(=O)[C@H](CCC(O)=O)NC(=O)[C@H](CCC(O)=O)NC(=O)[C@H](CC1=CC=CC=C1)NC(=O)[C@H](CC(O)=O)NC(=O)CNC(=O)[C@H](CC(N)=O)NC(=O)CNC(=O)CNC(=O)CNC(=O)CNC(=O)[C@@H]1CCCN1C(=O)[C@H](CCCNC(N)=N)NC(=O)[C@@H]1CCCN1C(=O)[C@H](N)CC1=CC=CC=C1)C(=O)N1CCC[C@H]1C(=O)N[C@@H](CCC(O)=O)C(=O)N[C@@H](CCC(O)=O)C(=O)N[C@@H](CC1=CC=C(O)C=C1)C(=O)N[C@@H](CC(C)C)C(O)=O
-14
2180.2853
2178.985813062
C98H138N24O33
InChI=1S/C98H138N24O33/c1-5-52(4)82(96(153)122-39-15-23-70(122)92(149)114-60(30-34-79(134)135)85(142)111-59(29-33-78(132)133)86(143)116-64(43-55-24-26-56(123)27-25-55)89(146)118-67(97(154)155)40-51(2)3)119-87(144)61(31-35-80(136)137)112-84(141)58(28-32-77(130)131)113-88(145)63(42-54-18-10-7-11-19-54)117-90(147)66(45-81(138)139)110-76(129)50-107-83(140)65(44-71(100)124)109-75(128)49-106-73(126)47-104-72(125)46-105-74(127)48-108-91(148)68-21-13-38-121(68)95(152)62(20-12-36-103-98(101)102)115-93(150)69-22-14-37-120(69)94(151)57(99)41-53-16-8-6-9-17-53/h6-11,16-19,24-27,51-52,57-70,82,123H,5,12-15,20-23,28-50,99H2,1-4H3,(H2,100,124)(H,104,125)(H,105,127)(H,106,126)(H,107,140)(H,108,148)(H,109,128)(H,110,129)(H,111,142)(H,112,141)(H,113,145)(H,114,149)(H,115,150)(H,116,143)(H,117,147)(H,118,146)(H,119,144)(H,130,131)(H,132,133)(H,134,135)(H,136,137)(H,138,139)(H,154,155)(H4,101,102,103)/t52-,57+,58-,59-,60-,61-,62-,63-,64-,65-,66-,67-,68-,69-,70-,82-/m0/s1
OIRCOABEOLEUMC-GEJPAHFPSA-N
901.57
543.33
218.54
66
37
28
2.78
11.88
-4
6
0
0
0
0
1
-0.76
-4.67
4.64e-02 g/l
7
(2S)-1-[(2S)-5-carbamimidamido-2-[(2S)-2-[(2R)-2-[(2S)-2-[(2S)-3-hydroxy-2-[(2S)-2-[(2S)-3-(1H-imidazol-4-yl)-2-{[(2S)-5-oxopyrrolidin-2-yl]formamido}propanamido]-3-(1H-indol-3-yl)propanamido]propanamido]-3-(4-hydroxyphenyl)propanamido]-4-methylpentanamido]-4-methylpentanamido]pentanoyl]-N-ethylpyrrolidine-2-carboxamide
leuprorelin
CCNC(=O)[C@@H]1CCCN1C(=O)[C@H](CCCNC(N)=N)NC(=O)[C@H](CC(C)C)NC(=O)[C@@H](CC(C)C)NC(=O)[C@H](CC1=CC=C(O)C=C1)NC(=O)[C@H](CO)NC(=O)[C@H](CC1=CNC2=C1C=CC=C2)NC(=O)[C@H](CC1=CNC=N1)NC(=O)[C@@H]1CCC(=O)N1
-2.4
1209.3983
1208.645462232
C59H84N16O12
InChI=1S/C59H84N16O12/c1-6-63-57(86)48-14-10-22-75(48)58(87)41(13-9-21-64-59(60)61)68-51(80)42(23-32(2)3)69-52(81)43(24-33(4)5)70-53(82)44(25-34-15-17-37(77)18-16-34)71-56(85)47(30-76)74-54(83)45(26-35-28-65-39-12-8-7-11-38(35)39)72-55(84)46(27-36-29-62-31-66-36)73-50(79)40-19-20-49(78)67-40/h7-8,11-12,15-18,28-29,31-33,40-48,65,76-77H,6,9-10,13-14,19-27,30H2,1-5H3,(H,62,66)(H,63,86)(H,67,78)(H,68,80)(H,69,81)(H,70,82)(H,71,85)(H,72,84)(H,73,79)(H,74,83)(H4,60,61,64)/t40-,41-,42-,43+,44-,45-,46-,47-,48-/m0/s1
GFIJNRVAKGFPGQ-LIJARHBVSA-N
429.04
327.24
125.24
32
16
16
9.49
11.92
1
6
0
0
0
0
1
1.04
-4.55
3.38e-02 g/l
14
(2S)-1-[(2S)-2-[(2S)-2-[(2R)-3-(tert-butoxy)-2-[(2S)-2-[(2S)-3-hydroxy-2-[(2S)-2-[(2S)-3-(1H-imidazol-5-yl)-2-{[(2S)-5-oxopyrrolidin-2-yl]formamido}propanamido]-3-(1H-indol-3-yl)propanamido]propanamido]-3-(4-hydroxyphenyl)propanamido]propanamido]-4-methylpentanamido]-5-[(diaminomethylidene)amino]pentanoyl]-N-(carbamoylamino)pyrrolidine-2-carboxamide
tetrahydrofolic acid
CC(C)C[C@H](NC(=O)[C@@H](COC(C)(C)C)NC(=O)[C@H](CC1=CC=C(O)C=C1)NC(=O)[C@H](CO)NC(=O)[C@H](CC1=CNC2=CC=CC=C12)NC(=O)[C@H](CC1=CN=CN1)NC(=O)[C@@H]1CCC(=O)N1)C(=O)N[C@@H](CCCN=C(N)N)C(=O)N1CCC[C@H]1C(=O)NNC(N)=O
-5.1
1269.4105
1268.641439486
C59H84N18O14
InChI=1S/C59H84N18O14/c1-31(2)22-40(49(82)68-39(12-8-20-64-57(60)61)56(89)77-21-9-13-46(77)55(88)75-76-58(62)90)69-54(87)45(29-91-59(3,4)5)74-50(83)41(23-32-14-16-35(79)17-15-32)70-53(86)44(28-78)73-51(84)42(24-33-26-65-37-11-7-6-10-36(33)37)71-52(85)43(25-34-27-63-30-66-34)72-48(81)38-18-19-47(80)67-38/h6-7,10-11,14-17,26-27,30-31,38-46,65,78-79H,8-9,12-13,18-25,28-29H2,1-5H3,(H,63,66)(H,67,80)(H,68,82)(H,69,87)(H,70,86)(H,71,85)(H,72,81)(H,73,84)(H,74,83)(H,75,88)(H4,60,61,64)(H3,62,76,90)/t38-,39-,40-,41-,42-,43-,44-,45+,46-/m0/s1
BLCLNMBMMGCOAS-URPVMXJPSA-N
495.89
325.84
130.74
33
18
17
9.36
10.91
1
6
0
0
0
0
1
0.30
-4.65
2.83e-02 g/l
27
(2R)-N-[(1S)-1-{[(1R)-1-{[(1S)-1-{[(1R)-1-{[(1S)-1-{[(1R)-1-{[(1S)-1-{[(1R)-1-{[(1S)-1-{[(1R)-1-{[(1S)-1-[(2-hydroxyethyl)carbamoyl]-2-(1H-indol-3-yl)ethyl]carbamoyl}-3-methylbutyl]carbamoyl}-2-(1H-indol-3-yl)ethyl]carbamoyl}-3-methylbutyl]carbamoyl}-2-(1H-indol-3-yl)ethyl]carbamoyl}-3-methylbutyl]carbamoyl}-2-(1H-indol-3-yl)ethyl]carbamoyl}-2-methylpropyl]carbamoyl}-2-methylpropyl]carbamoyl}-2-methylpropyl]carbamoyl}ethyl]-2-{2-[(2S)-2-formamido-3-methylbutanamido]acetamido}-4-methylpentanamide
(2R)-N-[(1S)-1-{[(1R)-1-{[(1S)-1-{[(1R)-1-{[(1S)-1-{[(1R)-1-{[(1S)-1-{[(1R)-1-{[(1S)-1-{[(1R)-1-{[(1S)-1-[(2-hydroxyethyl)carbamoyl]-2-(1H-indol-3-yl)ethyl]carbamoyl}-3-methylbutyl]carbamoyl}-2-(1H-indol-3-yl)ethyl]carbamoyl}-3-methylbutyl]carbamoyl}-2-(1H-indol-3-yl)ethyl]carbamoyl}-3-methylbutyl]carbamoyl}-2-(1H-indol-3-yl)ethyl]carbamoyl}-2-methylpropyl]carbamoyl}-2-methylpropyl]carbamoyl}-2-methylpropyl]carbamoyl}ethyl]-2-{2-[(2S)-2-formamido-3-methylbutanamido]acetamido}-4-methylpentanamide
CC(C)C[C@@H](NC(=O)CNC(=O)[C@@H](NC=O)C(C)C)C(=O)N[C@@H](C)C(=O)N[C@H](C(C)C)C(=O)N[C@@H](C(C)C)C(=O)N[C@H](C(C)C)C(=O)N[C@@H](CC1=CNC2=C1C=CC=C2)C(=O)N[C@H](CC(C)C)C(=O)N[C@@H](CC1=CNC2=C1C=CC=C2)C(=O)N[C@H](CC(C)C)C(=O)N[C@@H](CC1=CNC2=C1C=CC=C2)C(=O)N[C@H](CC(C)C)C(=O)N[C@@H](CC1=CNC2=C1C=CC=C2)C(=O)NCCO
5.96
1811.253
1810.033419343
C96H135N19O16
InChI=1S/C96H135N19O16/c1-50(2)36-71(105-79(118)48-102-93(128)80(54(9)10)103-49-117)86(121)104-58(17)84(119)113-82(56(13)14)95(130)115-83(57(15)16)96(131)114-81(55(11)12)94(129)112-78(43-62-47-101-70-33-25-21-29-66(62)70)92(127)108-74(39-53(7)8)89(124)111-77(42-61-46-100-69-32-24-20-28-65(61)69)91(126)107-73(38-52(5)6)88(123)110-76(41-60-45-99-68-31-23-19-27-64(60)68)90(125)106-72(37-51(3)4)87(122)109-75(85(120)97-34-35-116)40-59-44-98-67-30-22-18-26-63(59)67/h18-33,44-47,49-58,71-78,80-83,98-101,116H,34-43,48H2,1-17H3,(H,97,120)(H,102,128)(H,103,117)(H,104,121)(H,105,118)(H,106,125)(H,107,126)(H,108,127)(H,109,122)(H,110,123)(H,111,124)(H,112,129)(H,113,119)(H,114,131)(H,115,130)/t58-,71+,72+,73+,74+,75-,76-,77-,78-,80-,81+,82+,83-/m0/s1
NDAYQJDHGXTBJL-MWWSRJDJSA-N
519.89
492.33
194.73
50
16
20
11.56
0
8
0
0
0
0
1
4.38
-5.67
3.90e-03 g/l
35
(2R)-2-{[(2S)-1-[(4R,7S,10S,13S,16S)-13-benzyl-10-(2-carbamoylethyl)-7-(carbamoylmethyl)-16-[(4-hydroxyphenyl)methyl]-6,9,12,15,18-pentaoxo-1,2-dithia-5,8,11,14,17-pentaazacycloicosane-4-carbonyl]pyrrolidin-2-yl]formamido}-5-carbamimidamido-N-(carbamoylmethyl)pentanamide
tigecycline
NC(=O)CC[C@@H]1NC(=O)[C@H](CC2=CC=CC=C2)NC(=O)[C@H](CC2=CC=C(O)C=C2)NC(=O)CCSSC[C@H](NC(=O)[C@H](CC(N)=O)NC1=O)C(=O)N1CCC[C@H]1C(=O)N[C@H](CCCNC(N)=N)C(=O)NCC(N)=O
-6.1
1069.22
1068.426955905
C46H64N14O12S2
InChI=1S/C46H64N14O12S2/c47-35(62)15-14-29-40(67)58-32(22-36(48)63)43(70)59-33(45(72)60-18-5-9-34(60)44(71)56-28(8-4-17-52-46(50)51)39(66)53-23-37(49)64)24-74-73-19-16-38(65)54-30(21-26-10-12-27(61)13-11-26)41(68)57-31(42(69)55-29)20-25-6-2-1-3-7-25/h1-3,6-7,10-13,28-34,61H,4-5,8-9,14-24H2,(H2,47,62)(H2,48,63)(H2,49,64)(H,53,66)(H,54,65)(H,55,69)(H,56,71)(H,57,68)(H,58,67)(H,59,70)(H4,50,51,52)/t28-,29+,30+,31+,32+,33+,34+/m1/s1
NFLWUMRGJYTJIN-PNIOQBSNSA-N
435.41
279.78
104.78
19
15
14
9.5
11.77
1
4
0
0
0
0
1
-1.04
-3.99
1.10e-01 g/l
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Drug Experimental Properties

Drug properties that have been experimentally proven. Experimental drug properties are stored in the drug_experimental_properties table.

drug_id
melting_point
boiling_point
water_solubility
radioactivity
hydrophobicity
isoelectric_point
logp
logs
caco2_permeability
pka
1
65 °C
Soluble
3.7
2
61 °C (FAB fragment), 71 °C (whole mAb)
-0.413
8.48
3
67 °C
-0.083
4.58
4
-0.301
5.45
5
71 °C (whole mAb)
-0.529
7.89
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Drug Mappings

Drug mappings provide codes and identifiers from ATC, ATCVet and MeSH vocabularies that match a drug in DrugBank.

drug_id
code
vocabulary
vocabulary_level
direct
title
1
B
ATC
1
0
BLOOD AND BLOOD FORMING ORGANS
1
B01
ATC
2
0
ANTITHROMBOTIC AGENTS
1
B01A
ATC
3
0
ANTITHROMBOTIC AGENTS
1
B01AE
ATC
4
0
Direct thrombin inhibitors
1
QB
ATCvet
1
0
BLOOD AND BLOOD FORMING ORGANS
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Drug Predicted ADMET Properties

Predicted ADMET drug properties are stored in the drug_predicted_admet_properties table. Each row represents the properties for a single drug.

drug_id
caco2
caco2_probability
bbb
bbb_probability
hia
hia_probability
p_glycoprotein_substrate
p_glycoprotein_substrate_probability
p_glycoprotein_inhibitor_1
p_glycoprotein_inhibitor_1_probability
p_glycoprotein_inhibitor_2
p_glycoprotein_inhibitor_2_probability
renal_organic_cation_transporter
renal_organic_cation_transporter_probability
cyp450_2c9_substrate
cyp450_2c9_substrate_probability
cyp450_2d6_substrate
cyp450_2d6_substrate_probability
cyp450_3a4_substrate
cyp450_3a4_substrate_probability
cyp450_1a2_substrate
cyp450_1a2_substrate_probability
cyp450_2c9_inhibitor
cyp450_2c9_inhibitor_probability
cyp450_2d6_inhibitor
cyp450_2d6_inhibitor_probability
cyp450_2c19_inhibitor
cyp450_2c19_inhibitor_probability
cyp450_3a4_inhibitor
cyp450_3a4_inhibitor_probability
cyp_inhibitory_promiscuity
cyp_inhibitory_promiscuity_probability
herg_inhibitor_1
herg_inhibitor_1_probability
herg_inhibitor_2
herg_inhibitor_2_probability
ames_toxicity
ames_toxicity_probability
carcinogenicity
carcinogenicity_probability
biodegradation
biodegradation_probability
rat_acute_toxicity
6
0
0.8319
0
0.996
1
0.8811
Substrate
0.8692
Non-inhibitor
0.647
Non-inhibitor
0.7858
Non-inhibitor
0.7959
Non-substrate
0.7558
Non-substrate
0.7957
Substrate
0.5794
Non-inhibitor
0.8977
Non-inhibitor
0.8331
Non-inhibitor
0.8894
Non-inhibitor
0.7784
Non-inhibitor
0.744
Low CYP Inhibitory Promiscuity
0.9357
Weak inhibitor
0.9307
Non-inhibitor
0.514
Non AMES toxic
0.7642
Non-carcinogens
0.8217
Not ready biodegradable
0.9705
3.1654
14
0
0.7772
0
0.8816
1
0.9771
Substrate
0.9016
Non-inhibitor
0.5834
Non-inhibitor
0.8342
Non-inhibitor
0.7673
Non-substrate
0.7534
Non-substrate
0.7806
Substrate
0.6353
Non-inhibitor
0.8265
Non-inhibitor
0.7506
Non-inhibitor
0.8835
Non-inhibitor
0.7254
Non-inhibitor
0.6347
Low CYP Inhibitory Promiscuity
0.9054
Weak inhibitor
0.8841
Inhibitor
0.5249
Non AMES toxic
0.5851
Non-carcinogens
0.6406
Not ready biodegradable
1.0
2.6730
35
0
0.7612
0
0.8866
1
0.7979
Substrate
0.8242
Non-inhibitor
0.7864
Non-inhibitor
0.9237
Non-inhibitor
0.5915
Non-substrate
0.7833
Non-substrate
0.7901
Non-substrate
0.5497
Non-inhibitor
0.8383
Non-inhibitor
0.7906
Non-inhibitor
0.8735
Non-inhibitor
0.765
Non-inhibitor
0.7663
Low CYP Inhibitory Promiscuity
0.9331
Weak inhibitor
0.83
Inhibitor
0.6036
Non AMES toxic
0.6679
Non-carcinogens
0.8428
Not ready biodegradable
0.9445
2.7183
50
0
0.748
0
0.9647
1
0.913
Substrate
0.8796
Non-inhibitor
0.8235
Inhibitor
0.6194
Non-inhibitor
0.6856
Non-substrate
0.7609
Non-substrate
0.7938
Substrate
0.6358
Non-inhibitor
0.7491
Non-inhibitor
0.6987
Non-inhibitor
0.8339
Non-inhibitor
0.7056
Inhibitor
0.6531
Low CYP Inhibitory Promiscuity
0.9001
Weak inhibitor
0.7601
Inhibitor
0.649
Non AMES toxic
0.6327
Non-carcinogens
0.7553
Not ready biodegradable
1.0
2.7014
91
0
0.6994
0
0.9659
1
0.8727
Substrate
0.8463
Inhibitor
0.8685
Non-inhibitor
0.5992
Non-inhibitor
0.9485
Non-substrate
0.8628
Non-substrate
0.8823
Substrate
0.6407
Non-inhibitor
0.9045
Non-inhibitor
0.923
Non-inhibitor
0.9265
Non-inhibitor
0.9026
Non-inhibitor
0.6112
Low CYP Inhibitory Promiscuity
0.9968
Weak inhibitor
0.9815
Non-inhibitor
0.9214
Non AMES toxic
0.9133
Non-carcinogens
0.8948
Not ready biodegradable
0.9244
2.8788
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Drug Synonyms

Other names or identifiers that are associated with this drug. Drug synonyms are stored in the drug_synonyms table. Each row denotes one synonym.

id
synonym
drug_id
score
language
coder
source
1
Hirudin variant-1
1
good
english
26
t-PA
9
good
english
27
t-plasminogen activator
9
good
english
28
tPA
9
good
english
36
Kinase (enzyme-activating), uro-urokinase
13
good
english
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Drugs

Drugs are stored in the drugs table. Many tables include a drug_id column. This indicates that the rows of that tables can be related the rows of the drugs table by matching the id and drug_id columns. In SQL, this operation is a JOIN.

id
type
drugbank_id
name
state
description
simple_description
clinical_description
therapeutically_significant
cas_number
protein_formula
protein_weight
investigational
approved
vet_approved
experimental
nutraceutical
illicit
withdrawn
moldb_mono_mass
moldb_inchi
moldb_inchikey
moldb_smiles
moldb_average_mass
moldb_formula
synthesis_patent_id
protein_weight_details
biotech_kind
2
BiotechDrug
DB00002
Cetuximab
liquid
Cetuximab is a recombinant chimeric human/mouse IgG1 monoclonal antibody that competitively binds to epidermal growth factor receptor (EGFR) and competitively inhibits the binding of epidermal growth factor (EGF).[A227973] EGFR is a member of the ErbB family of receptor tyrosine kinases found in both normal and tumour cells; it is responsible for regulating epithelial tissue development and homeostasis.[A228083] EGFR has been implicated in various types of cancer, as it is often overexpressed in malignant cells [A227973] and EGFR overexpression has been linked to more advanced disease and poor prognosis.[A227963] EGFR is often mutated in certain types of cancer and serves as a driver of tumorigenesis.[A228083] _In vitro_, cetuximab was shown to mediate anti-tumour effects in numerous cancer cell lines and human tumour xenografts.[A227963] Approved by the FDA in February 2004 under the brand name ERBITUX, cetuximab is used for the treatment of head and neck cancer and metastatic, KRAS wild-type colorectal cancer, and metastatic colorectal cancer with a BRAF V600E mutation.[A227963,L39045] It has also been investigated in advanced colorectal cancer, EGFR-expressing non-small cell lung cancer (NSCLC), and unresectable squamous cell skin cancer.[L31418] Cetuximab is administered via intravenous infusion and is used as monotherapy or in combination with other chemotherapies, including platinum agents, radiation therapy, [leucovorin], [fluorouracil], and [irinotecan].[L30448]
A medication used to treat various cancers, including cancer of the head and neck and colorectal cancer.
An endothelial growth factor receptor binding fragment used to treat colorectal cancer as well as squamous cell carcinoma of the head and neck.
1
205923-56-4
C6484H10042N1732O2023S36
145781.6
0
1
0
0
0
0
0
recombinant
5
BiotechDrug
DB00005
Etanercept
liquid
Dimeric fusion protein consisting of the extracellular ligand-binding portion of the human 75 kilodalton (p75) tumor necrosis factor receptor (TNFR) linked to the Fc portion of human IgG1.[L14862,A216522] The Fc component of etanercept contains the CH2 domain, the CH3 domain and hinge region, but not the CH1 domain of IgG1. Etanercept is produced by recombinant DNA technology in a Chinese hamster ovary (CHO) mammalian cell expression system. It consists of 934 amino acids. It is used to treat or manage a variety of inflammatory conditions including rheumatoid arthritis (RA), ankylosing spondylitis (AS), and juvenile idiopathic poly-articular arthritis (JIA).
A potent medication used to treat inflammatory conditions such as rheumatoid arthritis and psoriasis.
A protein therapy based on the binding fragment of the tumour necrosis factor alpha receptor used to treat severe rheumatoid arthritis and moderate to severe plaque psoriasis.
1
185243-69-0
C2224H3475N621O698S36
51234.9
1
1
0
0
0
0
0
07276477
Monomer
recombinant
268
SmallMoleculeDrug
DB00268
Ropinirole
solid
Ropinirole, also known as _ReQuip_, is a non-ergoline dopamine agonist used in Parkinson's disease and restless legs syndrome [FDA label], [A174547]. It is manufactured by GlaxoSmithKline Pharmaceuticals. Ropinirole was initially approved in 1997 by the FDA [FDA label] for the management of Parkinson's disease. In 2005, it was the first drug approved in the US for the management of primary moderate to severe restless legs syndrome [A174547]. In 2008, the extended-release capsules of ropinirole were approved, allowing for less frequent dosing, therefore increased compliance, and offering a similar side effect profile and efficacy to previous formulations of ropinirole [A35711].
A medication used to treat the symptoms of Parkinson's disease, which causes problems with movement and muscle control, and Restless Legs Syndrome, which causes leg discomfort and strong urges to move the legs.
A non-ergoline dopamine agonist used to treat the symptoms of Parkinson's disease and Restless Legs Syndrome.
1
91374-21-9
1
1
0
0
0
0
0
260.1888634
InChI=1S/C16H24N2O/c1-3-9-18(10-4-2)11-8-13-6-5-7-15-14(13)12-16(19)17-15/h5-7H,3-4,8-12H2,1-2H3,(H,17,19)
UHSKFQJFRQCDBE-UHFFFAOYSA-N
CCCN(CCC)CCC1=C2CC(=O)NC2=CC=C1
260.3746
C16H24N2O
4452808
1050
SmallMoleculeDrug
DB01050
Ibuprofen
solid
Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics.[A39074] The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin.[A39075] Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID.[A39076] On the available products, ibuprofen is administered as a racemic mixture. Once administered, the R-enantiomer undergoes extensive interconversion to the S-enantiomer _in vivo_ by the activity of the alpha-methylacyl-CoA racemase. In particular, it is generally proposed that the S-enantiomer is capable of eliciting stronger pharmacological activity than the R-enantiomer.[A39194]
A pain medication used to reduce fever, pain, and inflammation.
An NSAID and non-selective COX inhibitor used to treat mild-moderate pain, fever, and inflammation.
1
15687-27-1
0
1
0
0
0
0
0
206.13067982
InChI=1S/C13H18O2/c1-9(2)8-11-4-6-12(7-5-11)10(3)13(14)15/h4-7,9-10H,8H2,1-3H3,(H,14,15)
HEFNNWSXXWATRW-UHFFFAOYSA-N
CC(C)CC1=CC=C(C=C1)C(C)C(O)=O
206.2808
C13H18O2
6430
SmallMoleculeDrug
DB06429
Talnetant
solid
Talnetant (SB-223,412) is a neurokinin 3 receptor antagonist developed by GlaxoSmithKline, which is being researched for several different functions, primarily for irritable bowel syndrome and as a potential antipsychotic drug for the treatment of schizophrenia.
0
174636-32-9
1
0
0
0
0
0
0
382.168127958
InChI=1S/C25H22N2O2/c1-2-20(17-11-5-3-6-12-17)27-25(29)22-19-15-9-10-16-21(19)26-23(24(22)28)18-13-7-4-8-14-18/h3-16,20,28H,2H2,1H3,(H,27,29)
BIAVGWDGIJKWRM-UHFFFAOYSA-N
CCC(NC(=O)C1=C(O)C(=NC2=CC=CC=C12)C1=CC=CC=C1)C1=CC=CC=C1
382.4544
C25H22N2O2
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External Identifiers

Any other identifiers that might be linked to the drug. This often includes numerical codes used during research and development of the drug.

id
drug_id
identifier
16593
2
ABP-494
1562
2
BMS 564717
16602
2
C-225
1563
2
C225
16590
2
CMAB-009
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External Resource Identifiers

Identifiers used in other websites or databases providing information about this drug.

record_type
record_id
source
identifier
Drug
1
ChEMBL
CHEMBL1201666
Drug
1
Drugs Product Database (DPD)
11916
Drug
1
PharmGKB
PA450195
Drug
1
PubChem Substance
46507011
Drug
1
RxCUI
237057
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Organisms

Organisms are stored in the organisms table.

id
name
826
Abelson murine leukemia virus
1255
Acetobacter aceti
535
Achromobacter cycloclastes
1549
Achromobacter lyticus
985
Acidaminococcus fermentans (strain ATCC 25085 / DSM 20731 / VR4)
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Pharmacologies

Describes the use, mechanism of action, pharmacokinetics, pharmacodynamics, and physiological or biochemical effects in the body.

id
drug_id
indication
pharmacodynamics
mechanism_of_action
absorption
toxicity
protein_binding
metabolism
half_life
route_of_elimination
volume_of_distribution
clearance
1
1
Lepirudin is indicated for anticoagulation in adult patients with acute coronary syndromes (ACS) such as unstable angina and acute myocardial infarction without ST elevation. In patients with ACS, lepirudin is intended for use with [aspirin].[L41539] Lepirudin is also indicated for anticoagulation in patients with heparin-induced thrombocytopenia (HIT) and associated thromboembolic disease in order to prevent further thromboembolic complications.[L41539]
Lepirudin is a recombinant hirudin that acts as a highly specific thrombin inhibitor. Its activity is measured by anti-thrombin units (ATUs) that correspond to the amount of lepirudin required to neutralize a unit of the World Health Organization α-thrombin (89/588) standard. The activity of lepirudin is 16,000 ATU/mg.[L41539,L41569] A single molecule of lepirudin binds to a molecule of thrombin, blocking its thrombogenic activity. This drug increases activated partial thromboplastin time (aPTT) and PT (INR) values in a dose-dependent manner, and its mode of action is independent of antithrombin III.[L41539,L41569] Platelet factor 4 does not inhibit lepirudin.[L41539,L41569] The pharmacodynamic effect of lepirudin was evaluated by measuring an increase in aPTT. No saturable effect was observed at the highest tested dose (0.5 mg/kg, IV bolus).[L41539] Thrombin time was considered an unsuitable routine test for lepirudin monitoring due to the high values detected (200 seconds) even at low doses.[L41539] The concomitant use of thrombolytic therapy and lepirudin is not recommended due to the high risk of bleeding that may be life-threatening. In patients with a risk of bleeding, a physician should weigh the risks of lepirudin administration against its benefits. There is also an especially high risk of bleeding in patients who weigh less than 50 kg, and a lower dosage is required. Patients with renal impairment have a higher risk of hemorrhagic adverse events.[L41539]
Lepirudin is a direct thrombin inhibitor used as an anticoagulant in patients for whom heparin is contraindicated.[L41539,A3] Thrombin is a serine protease that participates in the blood-clotting cascade, and it is formed by the cleavage of pro-thrombin. Active thrombin cleaves fibrinogen and generates fibrin monomers that polymerize to form fibrin clots.[A246624] Lepirudin binds to the catalytic and substrate-binding sites of thrombin, forming a stable, irreversible and non-covalent complex.[A246609] This blocks the protease activity of thrombin and inhibits the coagulation process. Each molecule of lepirudin binds to a single molecule of thrombin,[L41539] and unlike [heparin], it is able to inhibit thrombin in both its clot-bound or free states.[A246609]
Lepirudin administered as a single intravenous bolus injection of 0.4 mg/kg in 9 healthy volunteers (male and female) resulted in a Cmax of 2924 ng/mL, a tmax of 0.17 h and an AUC0-∞ of 2500 ng•h/mL.[L41539] When 0.1, 0.15 and 0.2 mg/kg of lepirudin was administered as a single intravenous infusion over 6 hours in healthy male volunteers, lepirudin had a corresponding Cmax of 111, 203, and 2446 ng/mL and a corresponding AUC of 612, 1184, and 1446 ng•h/mL.[L41544] Bioavailability is 100% following injection. Also, it has been reported that following subcutaneous (sc) administration, the bioavailability of lepirudin is almost 100%.[A246609]
The acute toxicity of intravenous lepirudin was evaluated in mice (0.1-1000 mg/kg), rats (1-1000 mg/kg), and monkeys (1-100 mg/kg), and toxicity was not detected at the doses investigated.[L41539] The acute toxicity of lepirudin administered subcutaneously was also evaluated in mice (1-1250 mg/kg) and rats (1-500 mg/kg), and no toxicity was detected.[L41539] One rat (100 mg/kg) died of rapid blood loss after the subcutaneous administration of lepirudin. Reactions to local injections such as hemorrhages, hematomas and/or nodules were detected in mice and rats given subcutaneous doses of lepirudin equal or higher than 500 mg/kg and 10 mg/kg, respectively.[L41539] Chronic toxicity was evaluated in rats and monkeys given lepirudin for up to 3 months. Most of the effects observed were due to the antithrombotic action of lepirudin. After 3 months, hemosiderin deposits in the spleen and moderate sinus histiocytosis in the lymph node were observed in rats. In monkeys, external and internal hemorrhages and hematomas were detected.[L41539] Lepidurin was reported as not mutagenic.[L41539] Relative overdose may occur in patients with renal impairment, therefore, bolus dose and rate of infusion must be reduced in case of known or suspected renal insufficiency.[L41539] Excessively high activated partial thromboplastin time (aPTT) values suggest an overdose and a risk of bleeding. Lepirudin has no known antidote. In case of life-threatening bleeding and if excessive plasma levels of lepirudin are suspected: 1)stop the administration of lepirudin immediately, 2) determine aPTT and coagulation parameters, 3) determine hemoglobin, and prepare for a transfusion, 4) follow the treatment guidelines for patients with shock.[L41539] Hemofiltration or hemodialysis may be useful in case of overdose, based in single case reports and animal data.[L41539]
In human plasma, the protein binding of lepirudin was approximately 3%.[L41539]
As a polypeptide, lepirudin is expected to be metabolized by the sequential cleavage of amino acids by kidney exoproteases, which have carboxypeptidase and dipeptidase-like activity.[L41539,L41544] The C-terminal cleavage of lepirudin aminoacids (aminoacids 1 to 65) produces four metabolites with anti-thrombotic activity: M1 (aminoacids 1 to 64), M2 (aminoacids 1 to 63), M3 (aminoacids 1 to 62), and M4 (aminoacids 1 to 61).[L41544]
Lepirudin has an initial half-life of approximately 10 minutes, and in young healthy volunteers, it has a terminal half-time of 1.3 hours.[L41539] Lepirudin has a first-order elimination kinetic; plasma concentration increases proportionally as the lepirudin intravenous dose is increased. Elimination half-life values of up to 2 days were detected in patients with marked renal insufficiency (creatinine clearance < 15 mL/min).[L41539]
Lepirudin is mostly excreted through urine (48.3%). About 35% of lepirudin is excreted unchanged, while metabolites are found in a smaller proportion (2.5% of M1, 5.4% of M2, 3.9% of M3 and 1.6% of M4).[L41544]
The volume of distribution of lepirudin at steady state was 12.2 L in healthy young subjects (n=18, 18-60 years), 18.7 L in healthy elderly subjects (n=10, 65-80 years), 18.0 L in renally impaired subjects (n=16, creatinine clearance < 80 mL/min, and 32.1 L in heparin-induced thrombocytopenia patients (n=73).[L41539] The distribution of lepirudin is mainly restricted to extracellular fluids.[L41539]
The clearance of lepirudin is proportional to the glomerular filtration rate. On average, lepirudin clearance was 164 mL/min in healthy young subjects (n=18, 18-60 years) and 25% lower in women than in men. In healthy elderly subjects (n=10, 65-80 years), clearance was 139 mL/min, about 20% lower than in younger patients.[L41539] This is possibly due to the lower creatinine clearance in elderly patients. In renally impaired subjects (n=16, creatinine clearance < 80 mL/min), clearance was 61 mL/min, and in heparin-induced thrombocytopenia patients (n=73), it was 114 mL/min.[L41539]
2
2
Cetuximab indicated for the treatment of locally or regionally advanced squamous cell carcinoma of the head and neck in combination with radiation therapy. It is indicated for treating a recurrent locoregional disease or metastatic squamous cell carcinoma of the head and neck in combination with platinum-based therapy with fluorouracil. It is indicated for recurrent or metastatic squamous cell carcinoma of the head and neck progressing after platinum-based therapy.[L30448] Cetuximab is also indicated for K-Ras wild-type, EGFR-expressing, metastatic colorectal cancer as determined by an FDA-approved test in combination with FOLFIRI, a chemotherapy combination that includes [leucovorin], [fluorouracil], and [irinotecan]; in combination with irinotecan in patients who are refractory to irinotecan-based chemotherapy; or as monotherapy in patients who have failed oxaliplatin- and irinotecan-based chemotherapy or who are intolerant to irinotecan.[L30448] Additionally, cetuximab is also indicated for metastatic colorectal cancer that is BRAF V600E mutation-positive (as determined by an FDA-approved test) in combination with [encorafenib] but only after prior therapy.[L39045] Cetuximab is not indicated for the treatment of Ras-mutant colorectal cancer or when the results of the Ras mutation tests are unknown.[L30448]
Cetuximab is an anticancer agent that works by inhibiting the growth and survival of epidermal growth factor receptor (EGFR)-expressing tumour cells with high specificity and higher affinity than epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), which are natural ligands of EGFR.[L31418] Cetuximab works by inhibiting the growth and survival of EGFR-positive tumours.[A227963] _In vitro_, it promotes antibody-dependent cellular cytotoxicity (ADCC) against certain human tumour types. On the contrary, cetuximab does not exert its anti-tumour effects on human tumour xenografts lacking EGFR expression.[A227963, L30448] Cetuximab potentiates the cytotoxic effects of chemotherapeutics and radiation therapy when used in combination.[L30448] In human tumour xenograft models in mice, cetuximab and irinotecan synergistically inhibited the growth of orthotopic anaplastic thyroid carcinoma xenografts _in vitro_ and _in vivo_. Cetuximab potentiated the _in vitro_ anti-proliferative and pro-apoptotic effect of irinotecan and achieved 93% _in vivo_ inhibition of tumour growth when combined with irinotecan, compared to 77% and 79% inhibition when cetuximab and irinotecan were used alone, respectively.[A227978]
The epidermal growth factor receptor (EGFR) is a transmembrane glycoprotein and a type I receptor tyrosine kinase expressed on both normal and malignant cells. It has been investigated as a therapeutic target for anticancer treatment, as it is often upregulated in cancer types, including head and neck, colon, and rectal cancers.[L30448] When activated by its ligand, EGFR undergoes a conformational change and dimerization to form homodimers or heterodimers with another member of the ErbB family of receptors. Dimerization of EGFR activates the intracellular tyrosine kinase region of EGFR and promotes autophosphorylation, initiating a series of downstream signalling cascades, including cell differentiation, proliferation, migration, angiogenesis, and apoptosis. This EGFR signalling pathway is often dysregulated in cancer cells, leading to aberrant cell growth and enhanced cell survival.[L31418] Cetuximab is a monoclonal antibody that binds specifically to the EGFR on both normal and tumour cells to competitively inhibit the binding of epidermal growth factor (EGF) and other ligands that are produced by normal and tumour tissue epithelial cells.[A11, L30448] Upon binding to domain III of EGFR - which is the binding site for its growth factor ligands - cetuximab prevents the receptor from adopting an extended conformation and thereby inhibits EGFR activation, as well as phosphorylation and activation of receptor-associated kinases (MAPK, PI3K/Akt, Jak/Stat).[A11, A228078] Inhibition of the EGFR signalling pathway ultimately leads to inhibition of cell cycle progression, cell survival pathways, and tumour cell motility and invasion.[A227963] Cetuximab also induces cell apoptosis and decreases matrix metalloproteinase and vascular endothelial growth factor (VEGF) production.[A228078, L30448] _In vitro_, cetuximab was shown to inhibit tumour angiogenesis.[A227978] Binding of cetuximab to EGFR also results in internalization of the antibody-receptor complex, leading to an overall downregulation of EGFR expression.[A227973] K-ras is a small G-protein downstream of EGFR that plays an important role in promoting the EGFR signalling cascade: in some malignant cells, K-ras can acquire activating mutations in exon 2 [L31418] and thus be continuously active regardless of EGFR regulation.[L30448] Since mutant Ras proteins can isolate the pathway from the effect of EGFR, K-Ras mutations can render EGFR inhibitors like cetuximab ineffective in exerting anti-tumour effects.[L30448, L31418] Cetuximab is thus only limited in its use for K-Ras wild-type, EGFR-expressing cancers.[L30448]
After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.[L30448] Tmax is about 3 hours.[A227963]
The intravenous LD50 is > 300 mg/kg in mice and > 200 mg/kg in rats.[L31408] There is limited information on the overdose from cetuximab. In clinical trials, cetuximab was associated with serious and fatal infusion reactions, cardiopulmonary arrest or sudden death, and serious dermatologic toxicities. Pulmonary toxicities, such as interstitial lung disease, interstitial pneumonitis with non-cardiogenic pulmonary edema, and exacerbation of pre-existing fibrotic lung disease have been reported.[L30448]
There is no information available.
Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway.[A40006]
After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the mean half-life for cetuximab was approximately 112 hours, with a range of 63 to 230 hours.[L30448]
There is limited information available.
The volume of the distribution is about 2-3 L/m2 and is independent of dose.[L30448]
In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck, the estimated clearance rate was 0.103 L/h.[A228003] At doses ranging from 200 to 400 mg/m2, complete saturation of systemic clearance was observed. In a population pharmacokinetic study, female patients had a 25% lower intrinsic cetuximab clearance than male patients, although there was no evidence of the need for dose modification based on sex.[A227963]
3
3
Used as adjunct therapy in the treatment of cystic fibrosis.
Cystic fibrosis (CF) is a disease characterized by the retention of viscous purulent secretions in the airways. These thick secretions contribute both to reduced pulmonary function and to frequent pulmonary infection. Purulent pulmonary secretions of individuals with cystic fibrosis contain very high concentrations of extracellular DNA released by degenerating leukocytes that accumulate in response to these infections. Dornase alfa hydrolyzes the DNA in sputum of CF patients and reduces sputum viscosity and viscoelasticity. The enzyme does not appear to affect sputum in the absence of an inflammatory response to infection, nor does it affect the sputum of healthy individuals.
Dornase alfa is a biosynthetic form of human DNase I. The enzyme is involved in endonucleolytic cleavage of extracellular DNA to 5´-phosphodinucleotide and 5´-phosphooligonucleotide end products. It has no effect on intracellular DNA. Optimal activity is dependent on the presence of divalent cations such as calcium and magnesium. Extracellular DNA is a viscous anionic polymer and its breakdown appears to improve the viscosity and viscoelasticity of purulent sputum of individuals with CF, thus reducing airflow obstruction. Dornase alfa does not seem to have any effect on non-purulent sputum.
Studies in rats and monkeys after inhalation of dornase alfa shows very little systemic absorption (less than 15% for rats and less than 2% for monkeys). The results were also witnessed in patients. Dornase alfa is also associated with very low accumulation with no serum concentration greater than 10ng/mL observed no matter the dose administered. Bioavailability: mean sputum concentrations of dornase alfa can be measured after 15 minutes. Onset is achieved within 3 to 7 days. Peak concentrations are achieved after 9 days.
Adverse reactions occur at a frequency of < 1/1000 and are usually mild and transient in nature. Reported adverse effects include chest pain (pleuritic/non-cardiac), fever, dyspepsia, voice alteration (hoarseness), pharyngitis, dyspnea, laryngitis, rhinitis, decreased lung function, rash, urticaria, and conjunctivitis. There is no evidence of carcinogenic or mutagenic properties. The safety of dornase alfa has not been studied in pregnant women, nursing women and children under the age of 5 years old.
While no conclusive studies have yet been published, dornase alfa is expected to be metabolized by proteases in biofluids.
In studies in rats and monkeys, the initial volume of distribution is similar to the serum volume. Concentrations in sputum decline rapidly after inhalation.
Studies in rats indicate that, following aerosol administration, the disappearance half-life of dornase alfa from the lungs is 11 hours. In humans, sputum DNase levels declined below half of those detected immediately post-administration within 2 hours but effects on sputum rheology persisted beyond 12 hours.
4
4
For treatment of cutaneous T-cell lymphoma
Denileukin diftitox (Ontak) directs the cytocidal action of diphtheria toxin to cells which express the IL-2 receptor. The human IL-2 receptor exists in three forms, low (CD25), intermediate (CD122/CD132) and high (CD25/CD122/CD132) affinity. Malignant cells expressing one or more of the subunits of the IL-2 receptor are found in certain leukemias and lymphomas including cutaneous T-cell lymphoma (CTCL). Ontak interacts with the high affinity IL-2 receptor on the cell surface and inhibits cellular protein synthesis, resulting in cell death within hours.
Denileukin diftitox binds to the high-affinity IL-2 receptor complex. The IL-2 receptor (Tac) subunit is expressed on activated but not resting lymphocytes. The diphtheria toxin associated with Ontak then selectively kills the IL-2 bearing cells.
70-80 min
* 0.06 to 0.09 L/kg
* 0.6 - 2.0 mL/min/kg [Lymphoma]
5
5
Etanercept is indicated for the treatment of moderately to severely active rheumatoid arthritis in adults and in chronic moderate to severe plaque psoriasis in patients 4 years of age and older.[L14862,L45523] It is also used to manage signs and symptoms of polyarticular idiopathic arthritis and Juvenile Psoriatic Arthritis in those aged 2 years and older. Etanercept is also used to manage the symptoms of psoriatic arthritis and ankylosing spondylitis.[L48526]
Etanercept binds specifically to tumor necrosis factor (TNF) and thereby modulates biological processes that are induced or regulated by TNF.[L14862,A216522] Such processes or molecules affected include the level of adhesion molecules expressed, as well as serum levels of cytokines and matrix metalloproteinases.
There are two distinct receptors for TNF (TNFRs), a 55 kilodalton protein (p55) and a 75 kilodalton protein (p75). The biological activity of TNF is dependent upon binding to either cell surface receptor (p75 or p55).[A216522] Etanercept is a dimeric soluble form of the p75 TNF receptor that can bind to two TNF molecules, thereby effectively removing them from circulation. Notably, etancerpt is only capable of binding to the active trimeric form of TNF as its binding site is located in the cleft between subunits.[A77626]TNF is a naturally occurring cytokine that is involved in normal inflammatory and immune responses.[A216522] Increased levels of TNF are found in tissues and fluids of those with rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and plaque psoriasis.
Population pharmacokinetic modeling in adults with RA, AS, or who were healthy showed a subcutaneous bioavailability of 56.9% with a Ka of 0.0223/h.[A215352] Another model in pediatric JIA patients showed an increased Ka of 0.05/h with a high mean interindividual variability of 215%.[A215357] Cmax after a single 25 mg subcutaneous dose of Enbrel is reported as 1.1 mcg/L with a Tmax of 69 h.[L14862] Cmax after repeated dosing is reported as 2.4 mcg/L in adult RA patients with a dosage of 25 mg twice weekly and 2.1 mcg in pediatric JIA patients with a dosage of 0.4 mg/kg twice weekly.
No significant protein binding has been identified.
As etanercept is a fusion protein antibody, it is assumed to be metabolized via proteinases similarly to endogenous proteins.
Etanercept has a mean half-life of elimination of 102 hours in RA patients.[L14862] Population models have shown a mean half-life of 68 hours in healthy adults and 70.7-94.8 hours in pediatric JIA patients.[A215657,A215357]
Population pharmacokinetic modeling predicts a total Vd of 5.49 L with a peripheral compartment of 1.24 L in adults with RA and an apparent Vd with subcutaneous administration in pediatric JIA patients of 7.88 L.[A215352,A215357]
Etanercept has a mean apparent clearance of 160 mL/h in RA patients.[L14862] Population models predict a mean apparent clearance of 132 mL/h in healthy adults and 0.0576 L/h in pediatric JIA patients.[A215657,A215357]
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Drug Sequences

Describes the protein sequences for biologic therapeutic proteins.

id
header
chain
sequenceable_id
sequenceable_type
type
1900
DB00001 sequence
LTYTDCTESGQNLCLCEGSNVCGQGNKCILGSDGEKNQCVTGEGTPKPQSHNDGDFEEIPEEYLQ
1
Drug
PolypeptideSequence
1902
DB00004 sequence
MGADDVVDSSKSFVMENFSSYHGTKPGYVDSIQKGIQKPKSGTQGNYDDDWKGFYSTDNKYDAAGYSVDNENPLSGKAGGVVKVTYPGLTKVLALKVDNAETIKKELGLSLTEPLMEQVGTEEFIKRFGDGASRVVLSLPFAEGSSSVEYINNWEQAKALSVELEINFETRGKRGQDAMYEYMAQACAGNRVRRSVGSSLSCINLDWDVIRDKTKTKIESLKEHGPIKNKMSESPNKTVSEEKAKQYLEEFHQTALEHPELSELKTVTGTNPVFAGANYAAWAVNVAQVIDSETADNLEKTTAALSILPGIGSVMGIADGAVHHNTEEIVAQSIALSSLMVAQAIPLVGELVDIGFAAYNFVESIINLFQVVHNSYNRPAYSPGHKTHAPTSSSTKKTQLQLEHLLLDLQMILNGINNYKNPKLTRMLTFKFYMPKKATELKHLQCLEEELKPLEEVLNLAQSKNFHLRPRDLISNINVIVLELKGSETTFMCEYADETATIVEFLNRWITFCQSIISTLT
4
Drug
PolypeptideSequence
1903
Etanercept Sequence
LPAQVAFTPYAPEPGSTCRLREYYDQTAQMCCSKCSPGQHAKVFCTKTSDTVCDSCEDSTYTQLWNWVPECLSCGSRCSSDQVETQACTREQNRICTCRPGWYCALSKQEGCRLCAPLRKCRPGFGVARPGTETSDVVCKPCAPGTFSNTTSSTDICRPHQICNVVAIPGNASMDAVCTSTSPTRSMAPGAVHLPQPVSTRSQHTQPTPEPSTAPSTSFLLPMGPSPPAEGSTGDEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK
5
Drug
PolypeptideSequence
1905
Peginterferon alfa-2a sequence
CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE
8
Drug
PolypeptideSequence
1907
DB00010 sequence
YADAIFTNSYRKVLGQLSARKLLQDIMSRQ
10
Drug
PolypeptideSequence
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Unique Ingredient Identifiers

Describes the salt format of the drug. Beneficial to map directly to our database if you are using the UNII database.

unii
record_id
record_type
Y43GF64R34
1
Drug
29O079NTYT
1
Salt
PQX0D8J21J
2
Drug
953A26OA1Y
3
Drug
25E79B5CTM
4
Drug
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Salt Calculated Properties

These properties have been predicted by ChemAxon based on the inputed chemical structure.

salt_id
iupac_name
iupac_traditional_name
smiles
logp
average_mass
mono_mass
formula
inchi
inchikey
polar_surface_area
refractivity
polarizability
rotatable_bond_count
acceptor_count
donor_count
pka_strongest_acidic
pka_strongest_basic
physiological_charge
number_of_rings
bioavailability
rule_of_five
ghose_filter
veber_rule
mddr_like_rule
alogps_logp
alogps_logs
alogps_solubility
1
(4S,4aS,5aS,6S,12aS)-7-chloro-4-(dimethylamino)-3,6,10,12,12a-pentahydroxy-1,11-dioxo-1,4,4a,5,5a,6,11,12a-octahydrotetracene-2-carboxamide hydrochloride
demeclocycline hydrochloride
Cl.[H][C@]12C[C@@]3([H])[C@H](N(C)C)C(O)=C(C(N)=O)C(=O)[C@@]3(O)C(O)=C1C(=O)C1=C([C@H]2O)C(Cl)=CC=C1O
-3.2
501.31
500.0753211
C21H22Cl2N2O8
InChI=1S/C21H21ClN2O8.ClH/c1-24(2)14-7-5-6-10(16(27)12-9(25)4-3-8(22)11(12)15(6)26)18(29)21(7,32)19(30)13(17(14)28)20(23)31;/h3-4,6-7,14-15,25-26,28-29,32H,5H2,1-2H3,(H2,23,31);1H/t6-,7-,14-,15-,21-;/m0./s1
GVSJQNRGSCOSNJ-KBHRXELFSA-N
181.62
114.35
43.66
2
9
6
2.94
9.04
-1
4
0
0
0
0
0
-0.4
-2.9
5.30e-01 g/l
4
dimethyl[3-(10H-phenothiazin-10-yl)propyl]amine hydrochloride
biotin
Cl.CN(C)CCCN1C2=CC=CC=C2SC2=CC=CC=C12
3.93
320.88
320.111397079
C17H21ClN2S
InChI=1S/C17H20N2S.ClH/c1-18(2)12-7-13-19-14-8-3-5-10-16(14)20-17-11-6-4-9-15(17)19;/h3-6,8-11H,7,12-13H2,1-2H3;1H
JIVSXRLRGOICGA-UHFFFAOYSA-N
6.48
88.95
33.09
4
2
0
9.2
1
3
1
1
1
1
0
4.63
-4.1
2.07e-02 g/l
5
[3-(2-chloro-10H-phenothiazin-10-yl)propyl]dimethylamine hydrochloride
biotin
Cl.CN(C)CCCN1C2=CC=CC=C2SC2=C1C=C(Cl)C=C2
4.54
355.325
354.072424754
C17H20Cl2N2S
InChI=1S/C17H19ClN2S.ClH/c1-19(2)10-5-11-20-14-6-3-4-7-16(14)21-17-9-8-13(18)12-15(17)20;/h3-4,6-9,12H,5,10-11H2,1-2H3;1H
FBSMERQALIEGJT-UHFFFAOYSA-N
6.48
93.76
35.42
4
2
0
9.2
1
3
1
1
1
1
0
5.18
-4.9
4.17e-03 g/l
6
(2Z)-but-2-enedioic acid; 5-[(1R)-2-[(5,6-diethyl-2,3-dihydro-1H-inden-2-yl)amino]-1-hydroxyethyl]quinoline-2,8-diol
biotin
[H]\C(=C(/[H])C(O)=O)C(O)=O.[H][C@](O)(CNC1CC2=C(C1)C=C(CC)C(CC)=C2)C1=C2C=CC(O)=NC2=C(O)C=C1
4.05
508.5629
508.220951388
C28H32N2O7
InChI=1S/C24H28N2O3.C4H4O4/c1-3-14-9-16-11-18(12-17(16)10-15(14)4-2)25-13-22(28)19-5-7-21(27)24-20(19)6-8-23(29)26-24;5-3(6)1-2-4(7)8/h5-10,18,22,25,27-28H,3-4,11-13H2,1-2H3,(H,26,29);1-2H,(H,5,6)(H,7,8)/b;2-1-/t22-;/m0./s1
IREJFXIHXRZFER-PCBAQXHCSA-N
85.61
115.1
44.99
8
5
4
8.54
9.83
1
4
1
0
0
0
1
3.9
-4.7
7.95e-03 g/l
7
[2-(diphenylmethoxy)ethyl]dimethylamine hydrochloride
biotin
Cl.CN(C)CCOC(C1=CC=CC=C1)C1=CC=CC=C1
3.65
291.816
291.138992038
C17H22ClNO
InChI=1S/C17H21NO.ClH/c1-18(2)13-14-19-17(15-9-5-3-6-10-15)16-11-7-4-8-12-16;/h3-12,17H,13-14H2,1-2H3;1H
PCHPORCSPXIHLZ-UHFFFAOYSA-N
12.47
79.93
29.88
6
2
0
8.87
1
2
1
1
1
1
0
3.44
-3.5
7.52e-02 g/l
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Salts

Identifies the available salt forms of specific drugs.

id
drug_id
drugbank_id
name
cas
moldb_smiles
moldb_formula
moldb_inchi
moldb_inchikey
moldb_average_mass
moldb_mono_mass
1
618
DBSALT000040
Demeclocycline hydrochloride
64-73-3
Cl.[H][C@]12C[C@@]3([H])[C@H](N(C)C)C(O)=C(C(N)=O)C(=O)[C@@]3(O)C(O)=C1C(=O)C1=C([C@H]2O)C(Cl)=CC=C1O
C21H22Cl2N2O8
InChI=1S/C21H21ClN2O8.ClH/c1-24(2)14-7-5-6-10(16(27)12-9(25)4-3-8(22)11(12)15(6)26)18(29)21(7,32)19(30)13(17(14)28)20(23)31;/h3-4,6-7,14-15,25-26,28-29,32H,5H2,1-2H3,(H2,23,31);1H/t6-,7-,14-,15-,21-;/m0./s1
GVSJQNRGSCOSNJ-KBHRXELFSA-N
501.31
500.0753211
4
420
DBSALT000147
Promazine hydrochloride
53-60-1
Cl.CN(C)CCCN1C2=CC=CC=C2SC2=CC=CC=C12
C17H21ClN2S
InChI=1S/C17H20N2S.ClH/c1-18(2)12-7-13-19-14-8-3-5-10-16(14)20-17-11-6-4-9-15(17)19;/h3-6,8-11H,7,12-13H2,1-2H3;1H
JIVSXRLRGOICGA-UHFFFAOYSA-N
320.88
320.111397079
5
477
DBSALT000026
Chlorpromazine hydrochloride
69-09-0
Cl.CN(C)CCCN1C2=CC=CC=C2SC2=C1C=C(Cl)C=C2
C17H20Cl2N2S
InChI=1S/C17H19ClN2S.ClH/c1-19(2)10-5-11-20-14-6-3-4-7-16(14)21-17-9-8-13(18)12-15(17)20;/h3-4,6-9,12H,5,10-11H2,1-2H3;1H
FBSMERQALIEGJT-UHFFFAOYSA-N
355.325
354.072424754
6
5039
DBSALT000101
Indacaterol maleate
753498-25-8
[H]\C(=C(/[H])C(O)=O)C(O)=O.[H][C@](O)(CNC1CC2=C(C1)C=C(CC)C(CC)=C2)C1=C2C=CC(O)=NC2=C(O)C=C1
C28H32N2O7
InChI=1S/C24H28N2O3.C4H4O4/c1-3-14-9-16-11-18(12-17(16)10-15(14)4-2)25-13-22(28)19-5-7-21(27)24-20(19)6-8-23(29)26-24;5-3(6)1-2-4(7)8/h5-10,18,22,25,27-28H,3-4,11-13H2,1-2H3,(H,26,29);1-2H,(H,5,6)(H,7,8)/b;2-1-/t22-;/m0./s1
IREJFXIHXRZFER-PCBAQXHCSA-N
508.5629
508.220951388
7
1075
DBSALT000056
Diphenhydramine hydrochloride
147-24-0
Cl.CN(C)CCOC(C1=CC=CC=C1)C1=CC=CC=C1
C17H22ClNO
InChI=1S/C17H21NO.ClH/c1-18(2)13-14-19-17(15-9-5-3-6-10-15)16-11-7-4-8-12-16;/h3-12,17H,13-14H2,1-2H3;1H
PCHPORCSPXIHLZ-UHFFFAOYSA-N
291.816
291.138992038
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Salts Synonyms

Other names or identifies that are associated with this salt.

id
salt_id
synonym
1
120
Aciclovir sodium
2
258
Albuterol sulfate
3
898
Benztropine mesylate
4
491
Clomiphene citrate
5
990
Cromolyn sodium
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Showing 19 of 19 tables