1

1

1

2

1

3

1

4

1

5

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

2012-04-24

0

0

0

0

1

0

1

idn

0

0

0

0

0

0

0

0

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

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

50

(2S)-N-[(2S)-5-carbamimidamido-1-[(2S)-2-{[(1R)-1-carbamoylethyl]carbamoyl}pyrrolidin-1-yl]-1-oxopentan-2-yl]-2-[(2R)-5-(carbamoylamino)-2-[(2S)-2-[(2S)-2-[(2R)-2-[(2R)-3-(4-chlorophenyl)-2-[(2R)-2-acetamido-3-(naphthalen-2-yl)propanamido]propanamido]-3-(pyridin-3-yl)propanamido]-3-hydroxypropanamido]-3-(4-hydroxyphenyl)propanamido]pentanamido]-4-methylpentanamide

cetrorelix

CC(C)C[C@H](NC(=O)[C@@H](CCCNC(N)=O)NC(=O)[C@H](CC1=CC=C(O)C=C1)NC(=O)[C@H](CO)NC(=O)[C@@H](CC1=CN=CC=C1)NC(=O)[C@@H](CC1=CC=C(Cl)C=C1)NC(=O)[C@@H](CC1=CC2=CC=CC=C2C=C1)NC(C)=O)C(=O)N[C@@H](CCCNC(N)=N)C(=O)N1CCC[C@H]1C(=O)N[C@H](C)C(N)=O

-1.7

1431.038

1429.669818444

C70H92ClN17O14

InChI=1S/C70H92ClN17O14/c1-39(2)31-52(61(94)82-51(15-9-28-77-69(73)74)68(101)88-30-10-16-58(88)67(100)79-40(3)59(72)92)83-60(93)50(14-8-29-78-70(75)102)81-63(96)54(34-43-20-25-49(91)26-21-43)86-66(99)57(38-89)87-65(98)56(36-45-11-7-27-76-37-45)85-64(97)55(33-42-18-23-48(71)24-19-42)84-62(95)53(80-41(4)90)35-44-17-22-46-12-5-6-13-47(46)32-44/h5-7,11-13,17-27,32,37,39-40,50-58,89,91H,8-10,14-16,28-31,33-36,38H2,1-4H3,(H2,72,92)(H,79,100)(H,80,90)(H,81,96)(H,82,94)(H,83,93)(H,84,95)(H,85,97)(H,86,99)(H,87,98)(H4,73,74,77)(H3,75,78,102)/t40-,50-,51+,52+,53-,54+,55-,56-,57+,58+/m1/s1

SBNPWPIBESPSIF-MHWMIDJBSA-N

495.67

384.16

148.93

38

18

17

9.5

11.79

1

6

0

0

0

0

1

1.33

-5.31

6.94e-03 g/l

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

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

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

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

0

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

0

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

0

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

0

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

0

16593

2

ABP-494

1562

2

BMS 564717

16602

2

C-225

1563

2

C225

16590

2

CMAB-009

Drug

1

ChEMBL

CHEMBL1201666

Drug

1

Drugs Product Database (DPD)

11916

Drug

1

PharmGKB

PA450195

Drug

1

PubChem Substance

46507011

Drug

1

RxCUI

237057

826

Abelson murine leukemia virus

1255

Acetobacter aceti

535

Achromobacter cycloclastes

1549

Achromobacter lyticus

985

Acidaminococcus fermentans (strain ATCC 25085 / DSM 20731 / VR4)

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 C_max of 2924 ng/mL, a t_max of 0.17 h and an AUC_0-∞ 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 C_max 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] T_max 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

Denileukin diftitox was previously indicated for the treatment of adult patients with persistent or recurrent cutaneous T-cell lymphoma (CTCL) whose malignant cells express the CD25 component of the IL-2 receptor.[L26381] It is also indicated for the treatment of adult patients with relapsed or refractory Stage I-III CTCL after at least one prior systemic therapy.[L51254]

Denileukin diftitox is an anticancer drug with cytocidal actions on cancer cells.[L51254] Denileukin diftitox demonstrated the ability to deplete immunosuppressive regulatory T lymphocytes (T_regs) and antitumor activity through direct cytocidal action on IL-2R-expressing tumours.[L51254]

Denileukin diftitox is a fusion protein composed of truncated diphtheria toxin (DT), which is a cytocidal moiety, and the full-length sequence of interleukin-2 (IL-2), which acts as a ligand for the IL-2 receptor.[A264344] Denileukin diftitox is reported to bind to a high- or intermediate-affinity receptor.[A264344] Once the drug molecule binds to the IL-2 receptor, denileukin diftitox is internalized via receptor-mediated endocytosis in an acidified vesicle.[A15, A264344] After uptake into the cell, denileukin diftitox is proteolytically cleaved within the endosomes to release the enzymatically active portion of the DT. DT is translocated across the endosomal membrane into the cytosol to inhibit protein synthesis via ADP-ribosylation of elongation factor-2, ultimately resulting in cell death. The fragment of DT is translocated across the endosomal membrane into the cytosol where it inhibits protein synthesis via ADP-ribosylation of elongation factor-2, resulting in cell death.[A264344, L51254]

Following a single dose of denileukin diftitox 9 mcg/kg via one-hour infusion in patients with CTCL, the geometric mean (coefficient of variation [CV]%) maximum serum concentration (C_max) was 94.4 ng/mL (77%) and area under the concentration over time curve (AUC_0-inf) was 20700 ng x min/L (60%) on the first day of the first administration cycle. There is no accumulation after repeated daily dosing.[L51254]

There is limited information regarding the acute toxicity (LD₅₀) and overdose of denileukin diftitox.

Denileukin diftitox is expected to be metabolized into small peptides by catabolic pathways.[L51254]

The arithmetic mean (CV%) denileukin diftitox terminal half-life is 112 minutes (31%) on the first day of the first cycle.[L51254]

The geometric mean (CV%) volume of distribution of denileukin diftitox is 5.0 L (43%) on the first day of the first administration cycle.[L51254]

The geometric mean (CV%) clearance is 36.5 mL/min (73%) after the first dose of denileukin diftitox at the recommended dose level.[L51254]

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]

1900

DB00001 sequence

LTYTDCTESGQNLCLCEGSNVCGQGNKCILGSDGEKNQCVTGEGTPKPQSHNDGDFEEIPEEYLQ

1

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

1908

DB00011 sequence

CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE

11

Drug

PolypeptideSequence

Y43GF64R34

1

Drug

29O079NTYT

1

Salt

PQX0D8J21J

2

Drug

953A26OA1Y

3

Drug

25E79B5CTM

4

Drug

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

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

1

120

Aciclovir sodium

2

258

Salbutamol sulfate

3

898

Benztropine mesylate

4

491

Clomiphene citrate

5

990

Cromolyn sodium