pharmacokinetics

Vardenafil (Vivanza) is an oral therapy for the treatment of erectile dysfunction. It is a selective inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5). Penile erection is a hemodynamic process initiated by the relaxation of smooth muscle in the corpus cavernosum and its associated arterioles. During sexual stimulation, nitric oxide is released from nerve endings and endothelial cells in the corpus cavernosum. Nitric oxide activates the enzyme guanylate cyclase resulting in increased synthesis of cyclic guanosine monophosphate (cGMP) in the smooth muscle cells of the corpus cavernosum. The cGMP in turn triggers smooth muscle relaxation, allowing increased blood flow into the penis, resulting in erection. The tissue concentration of cGMP is regulated by both the rates of synthesis and degradation via phosphodiesterases (PDEs). The most abundant PDE in the human corpus cavernosum is the cGMPspecific phosphodiesterase type 5 (PDE5); therefore, the inhibition of PDE5 enhances erectile function by increasing the amount of cGMP.

Vardenafil hydrochloride is a New Phosphodiesterase Type 5(PDE5) Inhibitor, in the Treatment of Erectile Dysfunction in Men With Diabetes

ML400 (CID73050863) is an allosteric inhibitor of LMPTP with an EC50 of 1μM. ML400 displays good cell-based activity and rodent pharmacokinetics.

1588-A4 (ARS-1620 Intermediate) is an intermediate of ARS-1620 which is an atropisomeric selective KRASG12C inhibitor with desirable pharmacokinetics.

Erlotinib-13C6 (CP-358774-13C6) is a 13C-labeled Erlotinib. Erlotinib is a directly acting EGFR tyrosine kinase inhibitor, with an IC50 of 2 nM for human EGFR[1]. Erlotinib reduces EGFR autophosphorylation in intact tumor cells with an IC50 of 20 nM. Erlotinib is used for the treatment of non-small cell lung cancer[1].Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process[2]. [1]. Moyer JD, et al. Induction of apoptosis and cell cycle arrest by CP-358,774, an inhibitor of epidermal growth factor receptor tyrosine kinase. Cancer Res. 1997, 57(21), 4838-4848.[2]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.

NNMT-IN-4 (compound 38) is a selective, uncompetitive inhibitor of nicotinamide N-methyltransferase (NNMT) with in vitro biochemical and cell-based assay IC50 values of 42 nM and 38 nM, respectively. It demonstrates favorable pharmacokinetics/pharmacodynamics (PK/PD) and safety profiles, excellent oral bioavailability, and promising pharmaceutical properties. NNMT-IN-4 serves as an in vivo chemical probe for NNMT [1].

Vardenafil dihydrochloride (Levitra) is a new type PDE inhibitor with IC50 of 0.7 and 180 nM for PDE5 and PDE1, respectively.

PROTAC BRD9 Degrader-7 is a selective and orally active BRD9 degrader with a DC50 of 1.02 nM and demonstrates superior pharmacokinetics, evidenced by a Cmax of 3436.95 ng/mL [1].

NS6180 is a potent and selective KCa3.1 channel inhibitor(IC50= 9 nM). It prevents T-cell activation and inflammation.

N-Desethyl Bimatoprost (17-phenyl trinor PGF2α amide) is an F-series PG analog in which the C-1 carboxyl group has been modified to an unsubstituted amide. PG esters have been shown to have ocular hypotensive activity. PG N-ethyl amides were recently introduced as alternative PG hypotensive prodrugs. Although it has been claimed that PG amides are not converted to the free acids in vivo, studies have shown that bovine and human corneal tissue converts the amides of various PGs to the free acids with a conversion efficiency of about 10-20% relative to the hydrolysis of isopropyl esters. 17-phenyl trinor PGF2α amide would be expected to show the typical intraocular effects of latanoprost, but with the much slower hydrolysis pharmacokinetics of the PG N-amides.

Paeoniflorgenin is a deglucosylated metabolite of Paeoniflorin[1]. [1]. Hsiu SL, et, al. A deglucosylated metabolite of paeoniflorin of the root of Paeonia lactiflora and its pharmacokinetics in rats. Planta Med. 2003 Dec; 69(12): 1113-8.

4-oxo Cyclophosphamide is an inactive metabolite of the alkylating agent cyclophosphamide .1,2It is formed from cyclophosphamide through a 4-hydroxycyclophosphamide intermediate by aldehyde dehydrogenases.2 1.Struck, R.F., Kirk, M.C., Mellett, L.B., et al.Urinary metabolites of the antitumor agent cyclophosphamideMol. Pharmacol.7(5)519-529(1971) 2.de Jonge, M.E., Huitema, A.D.R., Rodenhuis, S., et al.Clinical pharmacokinetics of cyclophosphamideClin. Pharmacokinet.44(11)1135-1164(2005)

Edoxaban impurity 6 is an impurity of Edoxaban. Edoxaban (DU-176) is a selective, potent and orally active factor Xa (FXa) inhibitor with Kis of 0.561 nM and 2.98 nM for free FXa and prothrombinase, respectively. Edoxaban is an anticoagulant agent and can be used for stroke prevention[1][2]. [1]. Furugohri T, et al. DU-176b, a potent and orally active factor Xa inhibitor: in vitro and in vivo pharmacological profiles. J Thromb Haemost. 2008 Sep;6(9):1542-9.[2]. Mendell J, Lee F, Chen S, The Effects of the Antiplatelet Agents, Aspirin and Naproxen, on Pharmacokinetics and Pharmacodynamics of the Anticoagulant Edoxaban, a Direct Factor Xa Inhibitor. J Cardiovasc Pharmacol. 2013 Apr 23.

Lipid 5 is an amino lipid compound that demonstrates proficient mRNA delivery in rodent and primate models, displaying favorable pharmacokinetics and minimal toxicity.

Celecoxib carboxylic acid is an inactive metabolite of the COX-2 inhibitor celecoxib .1,2It is formed from celecoxib primarily by the cytochrome P450 (CYP) isoform CYP2C9. 1.Liu, H., Huang, X., Shen, J., et al.Inhibitory mode of 1,5-diarylpyrazole derivatives against cyclooxygenase-2 and cyclooxygenase-1: Molecular docking and 3D QSAR analysesJ. Med. Chem.45(22)4816-4827(2002) 2.Kim, S.-H., Kim, D.-H., Byeon, J.-Y., et al.Effects of CYP2C9 genetic polymorphisms on the pharmacokinetics of celecoxib and its carboxylic acid metaboliteArch. Pharm. Res.40(3)382-390(2017)

BAY 1217224 is a neutral, non-prodrug Thrombin inhibitor with good oral pharmacokinetics.

Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1/2 by MEK1/2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0/G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg/kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013). Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1/2 by MEK1/2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0/G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg/kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3 References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013).

SBI-581 is an orally active, potent selective inhibitor of serine-threonine kinase TAO3, with an IC 50 of 42 nM. It effectively promotes the accumulation of TKS5α at RAB11-positive vesicles and inhibits the formation of invadopodia. Additionally, SBI-581 exhibits reasonable pharmacokinetics in mice when administered via IP injection, demonstrating significant antitumor activity [1].

Cap-dependent endonuclease-IN-9 is a potent (CEN) inhibitor with notable efficacy against the influenza virus and exhibits minimal cytotoxicity, enhanced in vivo pharmacokinetics, and robust pharmacodynamics. It effectively suppresses the RNA polymerase activity of A virus[1].

Pavurutamab (AMG-701) is a bispecific T-cell engager that targets CD3 and B-cell maturation antigens (BCMA), based on the extended half-life derived from Pacanalotamab. Its Fc region is engineered for improved pharmacokinetics, offering potential in immune regulation and the treatment of multiple myeloma (MM) [1] [2] [3] [4].

Omecamtiv mecarbil (CK-1827452) has been used in trials studying the treatment and basic science of Heart Failure, Echocardiogram, Pharmacokinetics, Chronic Heart Failure, and History of Chronic Heart Failure, among others.

p38 MAPK inhibitor (IC50 = 0.38 μM). Inhibits the release of IL-1β and TNF-α in a peripheral blood mononuclear cell (PBMC) assay (IC50 values are 0.039 and 0.16 μM respectively). Laufer et al (2003) Novel substituted pyridinyl imidazoles as potent anticytokine agents with low activity against hepatic cytochrome P450 enzymes. J.Med.Chem. 46 3230 PMID:12852754 |Kammerer et al (2007) Pharmacokinetics of ML3403 ({4-[5-(4-fluorophenyl)-2-methylsulfanyl-3H-imidazol-4-yl]-pyridin-2-yl}-(1-phenylethyl)-amine), a 4-pyridinylimidazole-type p38 mitogen-activated protein kinase inhibitor. Drug Metab.Dispos. 35 875 PMID:17344341

ARN24139 is a topoisomerase II poison (IC50= 7.3 μM in a topoisomerase II decatenation assay).1It inhibits proliferation of DU145, HeLa, and A549 cells (IC50s = 4.7, 3.8, and 3.1 μM, respectively). 1.Arencibia, J.M., Brindani, N., Franco-Ulloa, S., et al.Design, synthesis, dynamic docking, biochemical characterization, and in vivo pharmacokinetics studies of novel topoisomerase II poisons with promising antiproliferative activityJ. Med. Chem.63(7)3508-3521(2020)

(+)-Cevimeline hydrochloride hemihydrate ((+)-SNI-2011), a potent muscarinic receptor agonist, stands as a promising therapeutic candidate for treating xerostomia in Sjogren's syndrome. This compound has demonstrated a broad pharmacological profile across various systems including gastrointestinal, urinary, and reproductive, in animal models such as mice, rats, guinea pigs, rabbits, and dogs. Its metabolism was assessed in vitro using rat and dog liver microsomes, revealing that (+)-SNI-2011 is rapidly absorbed with peak plasma concentrations (Cmax) reached within one hour post-oral administration, followed by a decline with a half-life (t1/2) ranging from 0.4 to 1.1 hours. Bioavailability was recorded at 50% in rats and 30% in dogs. Metabolic analysis indicated species-specific differences, with rats producing both S- and N-oxidized metabolites and dogs only producing N-oxidized metabolites. Additionally, sex-based differences in pharmacokinetics were observed in rats but not in dogs. The in vitro study highlighted the involvement of cytochrome P450 (CYP) and flavin-containing monooxygenase (FMO) in the sulfoxidation and N-oxidation of SNI-2011, respectively, with CYP2D and CYP3A being primarily responsible for sulfoxidation in rat liver microsomes.

SC10914 is a highly potent PARP inhibitor (PARP1 IC50 = 7.87 nM) with potent anti-proliferative activity against human BRCA deficient tumor cells (MDA-MB-436, BRCA1 deficient, IC50 = 4.03 nM, Capan-1 BRCA2 deficient, IC50 = 11.66 nM) and PTEN deficient tumor cells (HGC-27,PTEN deficient, IC50 = 0.35 μM). SC10914 showed potent anti-tumor activity in BRCA1/2 mutant tumor models and better pharmacokinetics profile has the potential to be selected as the clinical candidate for the treatment of treatment of BRCA1/2 deficient cancers.

Dasiglucagon acetate is a novel glucagon analog for diabetic hypoglycemia therapy. Dasiglucagon acetate has demonstrated established solubility and stability in an aqueous formulation. Pharmacokinetics studies have shown dasiglucagon acetate to exhibit hi

Bavisant dihydrochloride hydrate (JNJ31001074AAC) is a highly selective, orally active antagonist of the human H3 receptor with a novel mechanism of action, involving wakefulness and cognition, with potential as a treatment for ADHD. in vivo: Mean change

Lerisetron is an antagonist of serotonin type 3 (5-HT3) receptor, with antiemetic activity.

MOZ-IN-3 (Compound 6j), a potent KAT6A (MOZ) acetyltransferase inhibitor with an IC50 of 30 nM, exhibits antitumor activity against multiple myeloid leukemia cell lines, including HL-60, U937, SKNO-1, and K562. This compound also demonstrates favorable metabolic stability and pharmacokinetics [1].

XY-06-007, a potent and selective bump-and-hole (B&H) PROTAC BRD4 BD1 L94V degrader, exhibits a DC50, 6 h of 10 nM specifically against BRD4 BD1 L94V without degrading off-targets. It also demonstrates favorable pharmacokinetics for in vivo studies [1].

Tofacitinib metabolite-1, a derivative of Tofacitinib, which is a JAK inhibitor, is employed in studies focused on the pharmacokinetics and metabolism of tofacitinib[1][2].

CAY10704 is a potent inhibitor of hepatitis C virus (HCV) infection (EC50 = 17 nM) that displays low cytotoxicity of virally-infected human hepatoma Huh7.5.1 cells (CC50 = 21.3 μM). It displays good pharmacokinetics in mice when delivered intraperitoneally, with preferential liver distribution without significant hepatotoxicity. CAY10704 is selective for HCV over dengue virus (EC50 = 4.62 μM).

Phosphoramide mustard cyclohexanamine is the major metabolite for Cyclophosphamide , with anticancer activitiy. Phosphoramide mustard cyclohexanamine induces DNA adduct formation in ovarian granulosa cells, induces DNA damage and elicits the ovarian DNA repair response[1][2]. Phosphoramide mustard cyclohexanamine causes cytotoxicity through forming cross-linked DNA adducts which inhibit DNA strand separation during replication[1].Phosphoramide mustard cyclohexanamine destroys rapidly dividing cells by forming NOR-G-OH, NOR-G and G-NOR-G adducts with DNA, potentially leading to DNA damage[1].Phosphoramide mustard cyclohexanamine (3-6 μM; 48 hours) reduces cell viability in rat spontaneously immortalized granulosa cells (SIGCs)[1].Phosphoramide mustard cyclohexanamine (3-6 μM; 24-48 hours) induces DNA adduct formation[1].Phosphoramide mustard cyclohexanamine (3-6 μM; 24-48 hours) induces ovarian DNA damage in rat ovaries[1].Phosphoramide mustard cyclohexanamine increases DNA damage responses (DDR) gene (Atm, Parp1, Prkdc, Xrcc6, Brca1, Rad51) mRNA expression level[1].Phosphoramide mustard cyclohexanamine (3-6 μM; 24-48 hours) increased DDR proteins[1]. Cell Viability Assay[1] Cell Line: SIGCs Phosphoramide mustard cyclohexanamine (2.1-20.7 mg/kg; i.p.; daily; for 5 days) inhibits subcutaneous tumor growth in rats[2].Phosphoramide mustard cyclohexanamine (86.0 mg/kg; i.v.) has a plasma disappearance half-life of 15.1 minutes[2]. Animal Model: Rat, subcutaneously implanted Walker 256 carcinosarcoma tumor[2] [1]. Shanthi Ganesan, et al. Phosphoramide mustard exposure induces DNA adduct formation and the DNA damage repair response in rat ovarian granulosa cells. Toxicol Appl Pharmacol. 2015 Feb 1; 282(3): 252-258. [2]. S Genka, et al. Brain and plasma pharmacokinetics and anticancer activities of cyclophosphamide and phosphoramide mustard in the rat. Cancer Chemother Pharmacol. 1990;27(1):1-7.

Ixazomib citrate, also known as MLN9708, is a prodrug of Ixazomib (MMLN-2238). MLN9708 is an orally bioavailable second generation proteasome inhibitor (PI) with potential antineoplastic activity. MLN9708, after hydrolyzing to pharmacologically active MLN2238 (ixazomib), is a next-generation proteasome inhibitor with demonstrated preclinical and clinical antimyeloma activity. MLN9708, compared with bortezomib, has improved pharmacokinetics, pharmacodynamics, and antitumor activity in preclinical studies.

Vardenafil hydrochloride trihydrate (BAY38-9456) is a new type PDE inhibitor with IC50 of 0.7 and 180 nM for PDE5 and PDE1, respectively.

FXIa-IN-6 is a potent FXIa inhibitor with selectivity against most of the relevant serine proteases ( K i = 0.3 nM). FXIa-IN-6 also demonstrated excellent pharmacokinetics (PK) profile (high oral bioavailability and low clearance) in multiple preclinical species.

Sulfachloropyrazine sodium(Sulfachloropyrazine) is an antiprotozoal,with antibacterial and anticoccidial effects

CAY10789 (compound 6) is a potent CysLT1R (cysteinyl leukotriene receptor 1) antagonist with an IC50 of 2.80 μM. CAY10789 is also a GPBAR1 (G-protein-coupled bile acid receptor 1) agonist with an EC50 of 3 μM. CAY10789 significantly decreases the adhesion of U937 cells to HAEC and decreases the expression of TNF-α. CAY10789 exhibits very promising metabolic stability and excellent pharmacokinetics. CAY10789 can be used in the study of colitis, metabolic syndromes, and other GPBAR1/CysLT1R-related diseases [1].

ML372 is a potent and selective SMN Modulator (EC50 = 12 nM, 325% increase inSMN2) with good potency, pharmacokinetics, tolerance, and CNS penetration.

Aditoprime (Aditoprim) is a selective inhibitor of bacterial dihydrofolate reductase (DHFR) that inhibits the transformation of dihydrofolic acid to tetrahydrofolic acid. Aditoprime shows good antibacterial activity and broad antimicrobial spectrum, and moreover, excellent pharmacokinetics. Aditoprime inhibits L.casei and E.coli DHFR with IC 50 of 520 and 47 nM, respectively [1] [2] [3].

Laropiprant (MK-0524) is a potent and selective antagonist of prostaglandin D2 (PGD2) receptor (DP) such as and DP/DP1 receptor(Ki = 0.57 nM) and TP Receptor(Ki = 2.95 nM).

Jaceosidin has anti-oxidative activity. Jaceosidin has anti-inflammatory activity, also a microglial inhibitor with anti-neuroinflammation activity. aceosidin has anticancer activity, modulates the ERK/ATM/Chk1/2 pathway, leading to inactivation of the Cd

4’-hydroxy Atomoxetine glucuronide is a metabolite of the norepinephrine transporter (NET) inhibitor atomoxetine .1It is formed from atomoxetine by glucuronidation of the intermediate metabolite 4-hydroxy atomoxetine.2 1.Todor, I., Popa, A., Neag, M., et al.Evaluation of a potential metabolism-mediated drug-drug interaction between atomoxetine and bupropion in healthy volunteersJ. Pharm. Pharm. Sci.19(2)198-207(2016) 2.Sauer, J.-M., Ring, B.J., and Witcher, J.W.Clinical pharmacokinetics of atomoxetineClin. Pharmacokinet.44(6)571-590(2005)

ABCG2-IN-1 (compound K2), an analog of Ko143, constitutes an orally active inhibitor targeting ABCG2 with an inhibitory concentration (IC50) of 0.13 μM. Demonstrating favorable oral pharmacokinetics in mice, ABCG2-IN-1 showcases promise for further research [1].

AChE-IN-7 (Compound 16) is a selective and effective acetylcholinesterase inhibitor with IC50 of 0.045 μM and 19.68 μ M for eeAChE and eeBuChE, respectively. AChE-IN-7 has high permeability of blood-brain barrier. AChE-IN-7 is safe in vivo and in vitro, and exhibits good overall pharmacokinetics and high bioavailability (F=55.5%).

Potent γ-secretase inhibitor (IC50 values are 1.2 and 6.2 nM in whole cell and cell-free assays, respectively). Reduces Aβ in brain, CSF and plasma in mice and guinea pigs. Lanz et al (2010) Pharmacodynamics and pharmacokinetics of the gamma-secretase inhibitor PF-3084014. J.Pharmacol.Exp.Ther. 334 269 PMID:20363853

Compounds 10B and 10C, functioning as cdk4/6 inhibitors, demonstrated low nanomolar activity, optimal antiproliferative effects, excellent metabolic properties, and acceptable pharmacokinetics targeting cdk4/6.

Labetalol (Apo-Labetalol) is a mixed alpha/beta-adrenergic antagonist.It is used to treat high blood pressure. It can be given by mouth for long term hypertension management or intravenously in severe hypertensive situations. The pharmacokinetics of labetalol is affected by the common CYP2C19 polymorphisms.

Despropylene gatifloxacin, a metabolite of AM-1155, exhibits potent antibacterial activity and has favorable pharmacokinetics [1].

COR659 is a GABAB positive allosteric modulator (PAM) . COR659 suppresses alcohol and chocolate self-administration in rats[1]. COR659 apparently exerts its effects via a composite mechanism, including positive allosteric modulation of the GABAB receptor and an action at the cannabinoid CB1 receptor[3]. COR659 (0, 2.5, 5 and 10 mg/kg) treatment is completely ineffective on lever-responding (FR10) for regular food pellets in food-deprived Wistar rats[1].COR659 is able to suppress lever-responding for a sucrose solution in sP rats and a chocolate solution in Wistar rats[2]. Animal Model: Male sP and Wistar rats[1]. [1]. Paola Maccioni, et al. Suppressing effect of COR659 on alcohol, sucrose, and chocolate self-administration in rats: involvement of the GABA B and cannabinoid CB 1 receptors. Psychopharmacology (Berl). 2017 Sep;234(17):2525-2543. [2]. Francesca Ferlenghi, et al. The GABA B receptor positive allosteric modulator COR659: In vitro metabolism, in vivo pharmacokinetics in rats, synthesis and pharmacological characterization of metabolically protected derivatives. Eur J Pharm Sci. 2020 Dec 1;155:105544. [3]. Paola Maccioni, et al. Anti-addictive properties of COR659 - Additional pharmacological evidence and comparison with a series of novel analogues. Alcohol. 2019 Mar;75:55-66.

Erlotinib is an epidermal growth factor receptor inhibitor. Erlotinib binds in a reversible fashion to the adenosine triphosphate (ATP) binding site of the receptor.

Erlotinib (NSC-718781) is an EGFR inhibitor (IC50: 2 nM). It is used for the treatment of non-small cell lung cancer.

Erlotinib hydrochloride (NSC 718781) is an EGFR inhibitor (IC50: 2 nM). It is used for the treatment of non-small cell lung cancer.

Erlotinib Hydrochloride inhibits purified EGFR kinase with an IC50 of 2 nM. Erlotinib D6 hydrochloride a deuterium labeled Erlotinib Hydrochloride.

Erlotinib is a directly acting inhibitor EGFR tyrosine kinase inhibitor with an IC50 of 2 nM for human EGFR. Erlotinib D6 is a deuterium labeled Erlotinib .