2-aminopurine profile

2-aminopurine is a synthetic adenine analog that can act as a base pair analog in DNA. It is commonly used as a fluorescent probe in molecular biology research because it exhibits unique spectral properties when incorporated into DNA. 2-aminopurine can be synthesized through various methods, including the reaction of 2-chloropurine with ammonia. It has been shown to exhibit mutagenic effects, primarily due to its ability to form base pairs with both adenine and guanine. This property makes it useful for studying DNA replication and repair mechanisms. The fluorescence properties of 2-aminopurine are sensitive to its environment, allowing researchers to investigate conformational changes, protein-DNA interactions, and DNA dynamics. Its ability to mimic adenine makes it a valuable tool for studying the structure and function of DNA and related processes.'

2-Aminopurine: A purine that is an isomer of ADENINE (6-aminopurine). [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

aminopurine : Any purine having at least one amino substituent. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

2-aminopurine : The parent compound of the 2-aminopurines, comprising a purine core carrying an amino substituent at the 2-position. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

ID Source	ID
PubMed CID	9955
CHEMBL ID	388594
CHEBI ID	479072
SCHEMBL ID	5631
MeSH ID	M0023189

Synonym
AC-13347
SDCCGMLS-0065821.P001
nsc-24129
purine, 2-amino-
nsc 24129
ccris 759
einecs 207-197-4
BIOMOLKI2_000050
MLS001333096
MLS001333095
smr000857109
1h-purin-2-amine
nsc24129
7h-purin-2-amine
sq 22,451
2-aminopurine
sq 22451
452-06-2
2-aminopurine, >=99%
BIOMOLKI_000044
NCGC00163382-01
9h-purin-2-amine
2bp ,
CHEMBL388594 ,
BMK1-E8
9h-purin-2-ylamine
bdbm50208875
2'-amino-purine
2-amino purine
chebi:479072 ,
aminopurine
AKOS006220998
HMS2230L13
AKOS015961157
CCG-100648
unii-o14b3u97fw
o14b3u97fw ,
isoadenine
191236-69-8
FT-0611268
aminopurine, 2-
sq-22451
(9h-purin-2-yl)amine
HMS3373E01
SCHEMBL5631
TS-00023
9h-purin-2-amine #
W-202796
mfcd00005566
DTXSID40196416
CS-W013358
849611-62-7
Z2786042704
Q209313
7h-purin-2-amine (9ci)
BCP32824
W13621
7h-purin-2-ylamine
citronellylcinnamate
7h-purin-2-amine(9ci)
HY-W012642
PD044966

Research Excerpts

Toxicity

Excerpt	Reference	Relevance
" The most common adverse experiences reported as related to study medication (famciclovir and placebo) were headache, nausea, and diarrhea."	( Safety of famciclovir in patients with herpes zoster and genital herpes. Boon, R; Jurewicz, R; Saltzman, R, 1994)	0.29
" There were no differences between groups in the incidence of adverse events."	( Efficacy and safety of famciclovir for treating mucocutaneous herpes simplex infection in HIV-infected individuals. Collaborative Famciclovir HIV Study Group. Aoki, FY; Lavender, EA; Martel, AY; Parsons, JE; Romanowski, B; Saltzman, RL, 2000)	0.31
" Four patients in the acyclovir plus placebo group did not complete the study protocol due to adverse events (n = 2), deviation from the protocol (n = 1), or loss to follow-up (n = 1)."	( Double-blind, randomized, acyclovir-controlled, parallel-group trial comparing the safety and efficacy of famciclovir and acyclovir in patients with uncomplicated herpes zoster. Chen, YS; Chiang, PC; Lee, SS; Lin, HH; Liu, YC; Shen, MC, 2004)	0.32
"3%) VZV-infected patients who received famciclovir three times a day experienced at least one adverse event."	( Pharmacokinetics and safety of famciclovir in children with herpes simplex or varicella-zoster virus infection. Abrams, B; Arguedas, A; Bomgaars, L; De León Castrejón, T; Hamed, K; Kaiser, G; Looby, M; Roberts, M; Rodriguez, A; Sáez-Llorens, X; Spigarelli, MG; Yogev, R; Zhou, W, 2009)	0.35
" Adverse events were generally mild and transient."	( Safety and pharmacokinetics of a single 1500-mg dose of famciclovir in adolescents with recurrent herpes labialis. Block, SL; Hamed, K; Waldmeier, F; Yogev, R, 2011)	0.37

Pharmacokinetics

Excerpt	Reference	Relevance
"The pharmacokinetic profile of penciclovir was determined after a single 500-mg dose of its oral precursor, famciclovir, in 9 healthy volunteers and in 14 patients with chronic hepatic disease."	( Pharmacokinetics of famciclovir in subjects with chronic hepatic disease. Audet, PR; Boike, SC; Fairless, A; Freed, MI; Ilson, BE; Jorkasky, DK; Pue, M; Zariffa, N, 1994)	0.29
" The possibility of a pharmacokinetic interaction between the anti-viral agent, famciclovir and allopurinol has been investigated in twelve healthy male volunteers following a single oral dose of famciclovir (500 mg) in the presence and absence of steady-state levels of allopurinol (300 mg)."	( Lack of a pharmacokinetic interaction between oral famciclovir and allopurinol in healthy volunteers. Fowles, SE; Laroche, J; Pratt, SK; Prince, WT, 1994)	0.29
" Plasma and urine concentrations of penciclovir and its 6-deoxy precursor, BRL 42359, were determined and penciclovir plasma concentration-time data submitted to model-independent pharmacokinetic analysis."	( Linear pharmacokinetics of penciclovir following administration of single oral doses of famciclovir 125, 250, 500 and 750 mg to healthy volunteers. Fairless, AJ; Fowles, S; Georgiou, P; Laroche, J; Pratt, SK; Prince, W; Pue, MA, 1994)	0.29
" Similar pharmacokinetic profiles for DXG were observed following either route of administration in serum, liver and brain."	( Biotransformation and pharmacokinetics of prodrug 9-(beta-D-1,3-dioxolan-4-yl)-2-aminopurine and its antiviral metabolite 9-(beta-D-1,3-dioxolan-4-yl)guanine in mice. Boudinot, FD; Chu, CK; Manouilov, KK; Manouilova, LS; Schinazi, RF, 1997)	0.52
" In paediatric patients this may be difficult to achieve due to lack of pharmacokinetic studies, administration of small doses, changes in body composition, continuous growth, and development and maturation of organs and systems."	( The pharmacokinetics of antiviral therapy in paediatric patients. Eksborg, S, 2003)	0.32
" Several phase I studies were conducted in healthy volunteers over the course of clinical development to evaluate whether pharmacokinetic drug-drug interactions exist between emtricitabine and other nucleoside antivirals that are extensively eliminated by renal excretion."	( Pharmacokinetic evaluation of emtricitabine in combination with other nucleoside antivirals in healthy volunteers. Begley, JA; Blum, MR; Chittick, GE; Hui, J; Wang, LH; Zong, J, 2007)	0.34
" Pooled pharmacokinetic data were generated after single doses in 51 participants (approximately 12."	( Pharmacokinetics and safety of famciclovir in children with herpes simplex or varicella-zoster virus infection. Abrams, B; Arguedas, A; Bomgaars, L; De León Castrejón, T; Hamed, K; Kaiser, G; Looby, M; Roberts, M; Rodriguez, A; Sáez-Llorens, X; Spigarelli, MG; Yogev, R; Zhou, W, 2009)	0.35
"To develop a population pharmacokinetic model for penciclovir (famciclovir is a prodrug of penciclovir) in adults and children and suggest an appropriate dose for children."	( Population pharmacokinetics and optimal design of paediatric studies for famciclovir. Aarons, L; Graham, G; Kaiser, G; Looby, M; Matthews, I; Ogungbenro, K, 2009)	0.35
" Population pharmacokinetic modelling was undertaken in NONMEM version VI."	( Population pharmacokinetics and optimal design of paediatric studies for famciclovir. Aarons, L; Graham, G; Kaiser, G; Looby, M; Matthews, I; Ogungbenro, K, 2009)	0.35
"A population pharmacokinetic model of penciclovir in adults and children has been developed."	( Population pharmacokinetics and optimal design of paediatric studies for famciclovir. Aarons, L; Graham, G; Kaiser, G; Looby, M; Matthews, I; Ogungbenro, K, 2009)	0.35
" The concentrations of penciclovir declined in a biphasic manner after the peak concentration was attained."	( Pharmacokinetics of penciclovir after oral administration of its prodrug famciclovir to horses. Kondo, T; Kurosawa, M; Matsumura, T; Nagata, S; Nemoto, M; Tsujimura, K; Yamada, M; Yamanaka, T, 2010)	0.36
" Seventeen infants were included in the pharmacokinetic analysis; one infant experienced immediate emesis and was excluded."	( Single-dose pharmacokinetics of famciclovir in infants and population pharmacokinetic analysis in infants and children. Blumer, J; Hamed, K; Kaiser, G; Rodriguez, A; Sallas, W; Sánchez, PJ, 2010)	0.36
"OBJECTIVES To determine, following oral administration of famciclovir, pharmacokinetic (PK) parameters for 2 of its metabolites (penciclovir and BRL42359) in plasma and tears of healthy cats so that famciclovir dosage recommendations for the treatment of herpetic disease can be optimized."	( Pharmacokinetic modeling of penciclovir and BRL42359 in the plasma and tears of healthy cats to optimize dosage recommendations for oral administration of famciclovir. Knych, HK; Maggs, DJ; Sebbag, L; Thomasy, SM; Woodward, AP, 2016)	0.43

Compound-Compound Interactions

Excerpt	Reference	Relevance
"Emtricitabine is a potent nucleoside reverse transcriptase inhibitor approved as a once-daily drug in combination with other antiretroviral agents for the treatment of HIV infection."	( Pharmacokinetic evaluation of emtricitabine in combination with other nucleoside antivirals in healthy volunteers. Begley, JA; Blum, MR; Chittick, GE; Hui, J; Wang, LH; Zong, J, 2007)	0.34
"A quencher-free and enzyme-free fluorescent sensor was proposed to simply and sensitively detect miRNA via the target catalyzed hairpin assembly (CHA) signal amplification in combination with 2-aminopurine (2-AP) molecular beacon (MBs)."	( 2-aminopurine probe in combination with catalyzed hairpin assembly signal amplification for simple and sensitive detection of microRNA. Cai, C; Chen, C; Chen, X; Gong, H; Liu, C; Lv, S, 2017)	2.09

Bioavailability

Excerpt	Reference	Relevance
"Potential oral prodrugs of the antiherpesvirus acyclonucleoside 9-[4-hydroxy-3-(hydroxymethyl)but-1-yl]guanine (1, BRL 39123) have been synthesized and evaluated for bioavailability of 1 in the blood of mice."	( Prodrugs of the selective antiherpesvirus agent 9-[4-hydroxy-3-(hydroxymethyl)but-1-yl]guanine (BRL 39123) with improved gastrointestinal absorption properties. Boyd, MR; Harnden, MR; Jarvest, RL; Sutton, D; Vere Hodge, RA, 1989)	0.28
"Famciclovir, a synthetic acyclic guanine derivative, is a prodrug which, after oral administration, is rapidly metabolised to the highly bioavailable antiviral compound penciclovir."	( Famciclovir. A review of its pharmacological properties and therapeutic efficacy in herpesvirus infections. Perry, CM; Wagstaff, AJ, 1995)	0.29
"Famciclovir is the well-absorbed oral form of penciclovir, an antiviral agent with potent activity against varicella-zoster virus (VZV) and herpes simplex virus (HSV-1) and 2 (HSV-2)."	( Famciclovir: review of clinical efficacy and safety. Cirelli, R; Herne, K; Lee, P; McCrary, M; Tyring, SK, 1996)	0.29
" The bioavailability of penciclovir, measured by urinary recovery, is approximately 60% and is not affected by food."	( The clinical pharmacokinetics of famciclovir. Gill, KS; Wood, MJ, 1996)	0.29
"Famciclovir is the well-absorbed oral form of penciclovir, a potent and selective antiviral agent, with activity against members of the herpesvirus family, including varicella-zoster virus (VZV), and herpes simplex virus-1 (HSV-1) and HSV-2."	( The pharmacological profile of famciclovir. Crumpacker, C, 1996)	0.29
" When administered orally, faMciclovir, the oral prodrug of PCV, is better absorbed than acyclovir, yielding an absolute bioavailability of PCV of 77%."	( Famciclovir for treatment of herpesvirus infections. Flaherty, JF; Luber, AD, 1996)	0.29
" Much of the current antiviral research focuses on providing drugs with (i) improved oral bioavailability and pharmacokinetics which permit less frequent oral or topical dosing for suppressive treatment of herpes simplex virus (HSV) infections, (ii) different mechanisms of action for synergic effects in treating resistant HSV infections in the immunocompromised host and (iii) improved efficacy."	( New therapeutic approaches to the alphaherpesvirus infections. Cassady, KA; Whitley, RJ, 1997)	0.3
" New antiviral drugs with improved oral bioavailability (famciclovir and valaciclovir) allow a better efficacy."	( [Drug clinics. How I treat zona]. Nikkels, AF; Piérard, GE, 1999)	0.3
" Famciclovir and valacyclovir offer improved oral bioavailability and convenient oral dosing schedules but are more expensive than acyclovir."	( Treatment of common cutaneous herpes simplex virus infections. Emmert, DH, 2000)	0.31
" Its bioavailability means that it can be taken less frequently than acyclovir, the only other approved herpes treatment."	( Drug effective against herpes. , 1996)	0.29
" Over the past two decades, the treatment of these conditions has been transformed by guanosine nucleoside antivirals such as valacyclovir (Valtrex, a highly bioavailable prodrug of acyclovir (Zovirax, and famciclovir (Famvir), a highly bioavailable prodrug of penciclovir (Denavir)."	( Valacyclovir in the treatment of herpes simplex, herpes zoster, and other viral infections. Brentjens, MH; Lee, P; Torres, G; Tyring, SK; Wu, JJ; Yeung-Yue, K, )	0.13
"Famciclovir, the well absorbed oral pro-drug of penciclovir, is effective in the treatment of herpes zoster when given three times daily."	( Once, twice, or three times daily famciclovir compared with aciclovir for the oral treatment of herpes zoster in immunocompetent adults: a randomized, multicenter, double-blind clinical trial. Ashton, R; Candaele, D; Decroix, J; Forszpaniak, C; Paulet, C; Shafran, SD; Tyring, SK; Wade, A, 2004)	0.32
" Subsequently, the orally bioavailable prodrugs valaciclovir and famciclovir have been introduced."	( Recent clinical experience with famciclovir--a "third generation" nucleoside prodrug. Beutner, K; Chakrabarty, A; Rauser, M; Tyring, SK, 2004)	0.32
"4 hours, respectively; and penciclovir bioavailability was 12."	( Pharmacokinetics of penciclovir in healthy cats following oral administration of famciclovir or intravenous infusion of penciclovir. Bales, JL; Ferrone, M; Maggs, DJ; Stanley, SD; Thomasy, SM; Whittem, T, 2012)	0.38
" Out of the six DAP-ANP analogues tested, analogue VI functionalized with a cyclopropyl group on the 6-amino position of the purine ring proves the most effective antiviral DAP-ANP analogue against PrV infection, aided by sufficient hydrophobic character to enhance bioavailability to its cellular target viral DNA-polymerase."	( Antiviral activities of 2,6-diaminopurine-based acyclic nucleoside phosphonates against herpesviruses: In vitro study results with pseudorabies virus (PrV, SuHV-1). Bartheldyova, E; Celechovska, H; Eyer, L; Fojtikova, M; Hubatka, F; Janeba, Z; Koudelka, S; Kovarcik, K; Kulich, P; Lipenska, I; Masek, J; Miller, AD; Neca, J; Plockova, J; Prochazka, L; Raska, M; Ruzek, D; Slany, M; Turanek, J; Turanek-Knotigova, P; Zouharova, D, 2016)	0.43

Dosage Studied

Excerpt	Relevance	Reference
" Mutational dose-response studies with X-rays, ethyl methanesulfonate (EMS), and ICR-191 were conducted in 4 of these revertant cell lines."	( Heritable alterations at the adenine phosphoribosyltransferase (APRT) locus in human lymphoblastoid cell lines. Amundson, SA; Fortunato, JE; Liber, HL, 1992)	0.28
" PDGF displays a steep dose-response relationship in the 1-5 ng/ml range."	( Activation of signal transduction pathways protects quiescent Balb/c-3T3 fibroblasts against death due to serum deprivation. Kikuchi, T; Tamm, I, 1991)	0.28
" Dose-response curves showed that AHA and HAP were about equally mutagenic at low doses but that AHA was more mutagenic than HAP at high doses."	( Effect of the uvs-2 allele of Neurospora crassa on the mutagenic potency of two N-hydroxylaminopurines and 2-aminopurine in the ad-3 forward-mutation test. Brockman, HE; de Serres, FJ; Hung, CY; Ong, T, 1989)	0.49
" These subsequent studies confirmed that, after oral dosing with famciclovir, more than half the dose was absorbed and rapidly converted to penciclovir."	( Selection of an oral prodrug (BRL 42810; famciclovir) for the antiherpesvirus agent BRL 39123 [9-(4-hydroxy-3-hydroxymethylbut-l-yl)guanine; penciclovir]. Boyd, MR; Harnden, MR; Jarvest, RL; Sutton, D; Vere Hodge, RA, 1989)	0.28
" Both 5 and its esters (14-17, 21, 22) and also 18 were well absorbed after oral administration and converted efficiently to 1, the diacetyl (14) and dipropionyl (16) esters providing concentrations of 1 in the blood that were more than 15-fold higher than those observed after dosing either 1 or its esters (25-27)."	( Prodrugs of the selective antiherpesvirus agent 9-[4-hydroxy-3-(hydroxymethyl)but-1-yl]guanine (BRL 39123) with improved gastrointestinal absorption properties. Boyd, MR; Harnden, MR; Jarvest, RL; Sutton, D; Vere Hodge, RA, 1989)	0.28
" The results of these and other experiments suggest that in these variants resistance to DAP is due to an altered aprt gene dosage and point to a possible genetic effect of colcemid and other aneuploidizing agents in somatic mammalian cells."	( Gene dosage mutants at adenine phosphoribosyltransferase locus induced by colcemid in Chinese hamster V79-AP4 cells. Colella, CM; Della Valle, G; Mariani, T; Peverali, AF; Piras, A; Rainaldi, G; Simi, S; Simili, M; Talarico, D; van Boxel, T, 1988)	0.27
" When dosing was reduced to once per day, both compounds were less effective at controlling the infection."	( Comparison of efficacies of famciclovir and valaciclovir against herpes simplex virus type 1 in a murine immunosuppression model. Field, HJ; Sutton, D; Tewari, D; Thackray, AM, 1995)	0.29
" On oral dosing of famciclovir to humans, only penciclovir and BRL 42359 can be detected consistently in the plasma; thus, attention was focused on the oxidation reaction."	( Role of aldehyde oxidase in the in vitro conversion of famciclovir to penciclovir in human liver. Chenery, RJ; Clarke, SE; Harrell, AW, 1995)	0.29
"Consideration should be given to modification of the dosing schedule of famciclovir from the usual 8-hour interval to a 12-hour interval for patients with moderate renal impairment (CLCR 30 to 59 ml/min/1."	( Pharmacokinetics of famciclovir in subjects with varying degrees of renal impairment. Audet, PR; Boike, SC; Fairless, A; Freed, MI; Ilson, BE; Jorkasky, DK; Pue, MA; Zariffa, N, 1994)	0.29
" Thus, famciclovir is now established as an effective treatment of immunocompetent patients with herpes zoster or genital herpes infection, particularly as famciclovir is administered in a convenient dosage regimen that may improve compliance compared with aciclovir."	( Famciclovir. A review of its pharmacological properties and therapeutic efficacy in herpesvirus infections. Perry, CM; Wagstaff, AJ, 1995)	0.29
" Dosage adjustment is required in the presence of renal impairment."	( Pharmacokinetics of new antiherpetic agents. Rolan, P, 1995)	0.29
" Dosage adjustment is not required for famciclovir in elderly patients with normal or mildly impaired renal function, and the extent of penciclovir availability is not affected by food."	( The pharmacological profile of famciclovir. Crumpacker, C, 1996)	0.29
" The dosage of famciclovir for herpes zoster in immunocompetent individuals is 500 mg po tid for 7 days; for recurrent genital herpes a dosage of 125 mg po bid for 5 days is recommended."	( Famciclovir for treatment of herpesvirus infections. Flaherty, JF; Luber, AD, 1996)	0.29
"Given its comparable efficacy, similar adverse effect profile, and less frequent dosing schedule than acyclovir, famciclovir represents a viable alternative for treatment of herpes zoster and for episodic therapy of recurrent genital herpes in immunocompetent adults."	( Famciclovir for treatment of herpesvirus infections. Flaherty, JF; Luber, AD, 1996)	0.29
" Much of the current antiviral research focuses on providing drugs with (i) improved oral bioavailability and pharmacokinetics which permit less frequent oral or topical dosing for suppressive treatment of herpes simplex virus (HSV) infections, (ii) different mechanisms of action for synergic effects in treating resistant HSV infections in the immunocompromised host and (iii) improved efficacy."	( New therapeutic approaches to the alphaherpesvirus infections. Cassady, KA; Whitley, RJ, 1997)	0.3
" Famciclovir and valacyclovir demonstrate superior pharmacokinetics compared with acyclovir and allow for less frequent daily dosing with higher achievable serum drug concentrations."	( Management of herpes simplex and varicella-zoster virus infections. Erlich, KS, 1997)	0.3
" With the completion of the first efficacy trials for each of these agents it has become apparent that, whilst less frequent dosing can he accomplished, it is not easy to significantly improve on the efficacy of aciclovir."	( Antiviral drugs in development for herpes zoster. Fiddian, AP, 1996)	0.29
" The pharmacokinetics of famciclovir allow a more convenient dosing schedule than the schedule used with acyclovir."	( Famciclovir: a new systemic antiviral agent for herpesvirus infections. Stott, GA, 1997)	0.3
" New areas of retinitis developed within the posterior pole despite treatment with the maximum dosage of acyclovir; thus, we used a new antiviral agent, famciclovir."	( Famciclovir for the treatment of acute retinal necrosis (ARN) syndrome. Figueroa, MS; Fortun, J; Garabito, I; Gutierrez, C, 1997)	0.3
" Famciclovir is effective in the suppression and treatment of HSV infections; however, no studies have examined the optimum dosing regimen for HSV prophylaxis in laser resurfacing."	( Famciclovir prophylaxis of herpes simplex virus reactivation after laser skin resurfacing. Alster, TS; Nanni, CA, 1999)	0.3
" Famciclovir and valacyclovir offer improved oral bioavailability and convenient oral dosing schedules but are more expensive than acyclovir."	( Treatment of common cutaneous herpes simplex virus infections. Emmert, DH, 2000)	0.31
" The prodrugs valacyclovir and famciclovir offer easier, less-frequent dosing than required for acyclovir."	( Progress in meeting today's demands in genital herpes: an overview of current management. Patel, R, 2002)	0.31
"Valacyclovir is the only oral antiviral agent approved for therapy of herpes labialis, the only antiviral drug approved for a 3-day course in the episodic treatment of recurrent genital herpes, as well as the only antiviral drug approved for once daily dosing for suppressive therapy."	( Valacyclovir in the treatment of herpes simplex, herpes zoster, and other viral infections. Brentjens, MH; Lee, P; Torres, G; Tyring, SK; Wu, JJ; Yeung-Yue, K, )	0.13
" Prophylactic oral antiviral agents are administered routinely to patients undergoing laser resurfacing to prevent postoperative HSV-1 eruptions; however, dosage and duration of treatment vary in the literature."	( Herpes simplex virus prophylaxis with famciclovir in patients undergoing aesthetic facial CO2 laser resurfacing. Bisaccia, E; Scarborough, D, 2003)	0.32
" The treatment for recurrent hepatitis B after liver transplantation includes increased dosage of lamivudine, application of famciclovir, and other liver protection measures."	( Prophylaxis and treatment of hepatitis B virus reinfection following liver transplantation. Huang, DS; Liang, TB; Wang, WL; Wu, J; Xu, X; Zheng, SS, 2002)	0.31
" Choice of therapy would then depend on convenience of dosing and cost."	( Antiviral treatment of genital herpes. Apoola, A; Radcliffe, K, 2004)	0.32
" These compounds offer high oral bioavailabilty and deliver acyclovir and penciclovir, respectively, to the target cells by means of more convenient dosing schedules."	( Recent clinical experience with famciclovir--a "third generation" nucleoside prodrug. Beutner, K; Chakrabarty, A; Rauser, M; Tyring, SK, 2004)	0.32
"In immunocompetent adults with recurrent genital herpes, a 5-day course of famciclovir at a dosage of 125 mg, 250 mg, or 500 mg twice per day was significantly more effective than was placebo in reducing the duration of viral shedding and symptoms and in accelerating lesion healing."	( Clinic-initiated, twice-daily oral famciclovir for treatment of recurrent genital herpes: a randomized, double-blind, controlled trial. Aoki, FY; Lassonde, M; Martel, AY; Sacks, SL; Shafran, SD, 2005)	0.33
" Although traditional therapy for a recurrent episode for healthy adults has consisted of twice-daily dosing for 5 days, recent studies have indicated that shorter courses of antiviral therapy are effective."	( Single-day, patient-initiated famciclovir therapy for recurrent genital herpes: a randomized, double-blind, placebo-controlled trial. Aoki, FY; Diaz-Mitoma, F; Gao, J; Gross, G; Hamed, K; Tyring, S, 2006)	0.33
" The factors influencing the choice of therapy, such as cost, ease of dosing and acyclovir resistance are also discussed."	( Genital herpes: antiviral therapy for symptom relief and prevention of transmission. Gupta, R; Wald, A, 2006)	0.33
" single-day bid famciclovir and placebo in the treatment of herpes labialis demonstrated single-dose famciclovir to be as efficacious as single-day bid dosing in time to healing of lesions and more efficacious than single-day bid famciclovir in time to resolution of pain and tenderness."	( Single-dose famciclovir for the treatment of herpes labialis. Hamed, K; Hull, C; Spruance, S; Tyring, S, 2006)	0.33
" Its pharmacokinetics allow for administration in a convenient dosing regimen compared with acyclovir, which may improve compliance."	( Famciclovir for the treatment of recurrent genital herpes: a clinical and pharmacological perspective. Aoki, FY; Vinh, DC, 2006)	0.33
" Convenient patient-initiated single-day (for recurrent genital herpes) and single-dose (for orolabial herpes) dosage regimens may contribute to treatment compliance, patient acceptability and subsequent treatment outcomes."	( Famciclovir: a review of its use in herpes zoster and genital and orolabial herpes. Lyseng-Williamson, KA; Simpson, D, 2006)	0.33
" Famciclovir has received single-day dosing indications for both of these entities."	( Famciclovir for cutaneous herpesvirus infections: an update and review of new single-day dosing indications. Chacko, M; Weinberg, JM, 2007)	0.34
"Penciclovir pharmacokinetics following oral famciclovir administration in cats appeared complex within the dosage range studied."	( Pharmacokinetics and safety of penciclovir following oral administration of famciclovir to cats. Maggs, DJ; Moulin, NK; Stanley, SD; Thomasy, SM, 2007)	0.34
" Whereas the diagnosis of this condition is often straightforward, choosing an appropriate drug (eg, acyclovir, valacyclovir hydrochloride, or famciclovir) and dosing regimen can be confusing in view of (1) competing clinical approaches to therapy; (2) evolving dosing schedules based on new research; (3) approved regimens of the Food and Drug Administration that may not match recommendations of the Centers for Disease Control and Prevention or of other experts; and (4) dissimilar regimens for oral and genital infections."	( The treatment of herpes simplex infections: an evidence-based review. Brodell, RT; Cernik, C; Gallina, K, 2008)	0.35
" More rigorous clinical trials are required to optimise the dosing regimen for safe and effective specific anti-herpes treatment in feline clinical medicine."	( Treatment of feline herpesvirus-1 associated disease in cats with famciclovir and related drugs. Graham, PG; Lessels, NS; Malik, R; Meek, M; Norris, JM; Power, H; Vitale, C; Webb, S, 2009)	0.35
" An eight-step weight-based dosing regimen was developed to optimize exposure in smaller children and was used in the 7-day multiple-dose safety phases of both studies, which enrolled 100 patients with confirmed/suspected viral infections."	( Pharmacokinetics and safety of famciclovir in children with herpes simplex or varicella-zoster virus infection. Abrams, B; Arguedas, A; Bomgaars, L; De León Castrejón, T; Hamed, K; Kaiser, G; Looby, M; Roberts, M; Rodriguez, A; Sáez-Llorens, X; Spigarelli, MG; Yogev, R; Zhou, W, 2009)	0.35
" An eight-step dosing regimen was derived that targeted exposure in infants and children 6 months to 12 years of age to match the penciclovir AUC seen in adults after a 500-mg dose of famciclovir."	( Single-dose pharmacokinetics of famciclovir in infants and population pharmacokinetic analysis in infants and children. Blumer, J; Hamed, K; Kaiser, G; Rodriguez, A; Sallas, W; Sánchez, PJ, 2010)	0.36
" Furthermore, the superior pharmacokinetics and more convenient dosing regimens with the use of valaciclovir and famciclovir clearly make them the preferred treatment option."	( Antivirals for management of herpes zoster including ophthalmicus: a systematic review of high-quality randomized controlled trials. de Kock, J; McDonald, EM; Ram, FS, 2012)	0.38
"Penciclovir pharmacokinetics following oral administration of famciclovir were nonlinear within the dosage range studied, likely because of saturation of famciclovir metabolism."	( Pharmacokinetics of penciclovir in healthy cats following oral administration of famciclovir or intravenous infusion of penciclovir. Bales, JL; Ferrone, M; Maggs, DJ; Stanley, SD; Thomasy, SM; Whittem, T, 2012)	0.38
" Six of 16 patients (37%) receiving long-term oral acyclovir had recurrent HSV, at least one case of which followed a growth spurt that caused the baseline dosage of acyclovir to become subtherapeutic."	( Pediatric herpes simplex of the anterior segment: characteristics, treatment, and outcomes. Colby, KA; Liu, S; Pavan-Langston, D, 2012)	0.38
" Oral acyclovir is effective, but the dosage must be adjusted as the child grows."	( Pediatric herpes simplex of the anterior segment: characteristics, treatment, and outcomes. Colby, KA; Liu, S; Pavan-Langston, D, 2012)	0.38
" However, drug concentrations were noninhibitory during 42% of the dosing cycle."	( Rapid viral expansion and short drug half-life explain the incomplete effectiveness of current herpes simplex virus 2-directed antiviral agents. Corey, L; Schiffer, JT; Swan, DA; Wald, A, 2013)	0.39
" In analyzing parallel-group trials by daily dose, no clear evidence was found of a dose-response relationship for any drug."	( Oral antiviral therapy for prevention of genital herpes outbreaks in immunocompetent and nonpregnant patients. Chosidow, O; Do, G; Le Cleach, L; Lebrun-Vignes, B; Maruani, A; Ravaud, P; Trinquart, L, 2014)	0.4
"OBJECTIVES To determine, following oral administration of famciclovir, pharmacokinetic (PK) parameters for 2 of its metabolites (penciclovir and BRL42359) in plasma and tears of healthy cats so that famciclovir dosage recommendations for the treatment of herpetic disease can be optimized."	( Pharmacokinetic modeling of penciclovir and BRL42359 in the plasma and tears of healthy cats to optimize dosage recommendations for oral administration of famciclovir. Knych, HK; Maggs, DJ; Sebbag, L; Thomasy, SM; Woodward, AP, 2016)	0.43
" Further studies are needed to assess whether a famciclovir dosage of 90 versus 40 mg/kg, PO, 3 times/d would result in increased efficacy and shorter treatment time."	( Oral administration of famciclovir for treatment of spontaneous ocular, respiratory, or dermatologic disease attributed to feline herpesvirus type 1: 59 cases (2006-2013). Freeman, KS; Kass, PH; Lim, CC; Maggs, DJ; Outerbridge, CA; Shull, O; Strom, AR; Thomasy, SM, 2016)	0.43

[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Role	Description
antimetabolite	A substance which is structurally similar to a metabolite but which competes with it or replaces it, and so prevents or reduces its normal utilization.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Class	Description
2-aminopurines	Any aminopurine having the amino substituent at the 2-position.
nucleobase analogue	A molecule that can substitute for a normal nucleobase in nucleic acids.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein	Taxonomy	Measurement	Average (µ)	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Chain A, Beta-lactamase	Escherichia coli K-12	Potency	10.0000	0.0447	17.8581	100.0000	AID485294
thioredoxin reductase	Rattus norvegicus (Norway rat)	Potency	15.8489	0.1000	20.8793	79.4328	AID588453
aldehyde dehydrogenase 1 family, member A1	Homo sapiens (human)	Potency	37.6505	0.0112	12.4002	100.0000	AID1030
IDH1	Homo sapiens (human)	Potency	0.4611	0.0052	10.8652	35.4813	AID686970
Guanine nucleotide-binding protein G	Homo sapiens (human)	Potency	11.2202	1.9953	25.5327	50.1187	AID624288
TAR DNA-binding protein 43	Homo sapiens (human)	Potency	39.8107	1.7783	16.2081	35.4813	AID652104
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)	IC50 (µMol)	341.6000	0.2800	3.6900	7.1000	AID155650
Xanthine dehydrogenase/oxidase	Homo sapiens (human)	IC50 (µMol)	200.0000	0.0013	2.8138	9.8200	AID287937
Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)	IC50 (µMol)	341.6000	7.1000	7.1000	7.1000	AID155650
Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)	IC50 (µMol)	341.6000	7.1000	7.1000	7.1000	AID155650
Phosphatidylinositol 4-kinase beta	Homo sapiens (human)	IC50 (µMol)	341.6000	0.0183	2.4510	7.1000	AID155650
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
phosphorylation	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
phosphatidylinositol biosynthetic process	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
signal transduction	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
modulation by host of viral process	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
phosphatidylinositol phosphate biosynthetic process	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
reorganization of cellular membranes to establish viral sites of replication	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
phosphatidylinositol-mediated signaling	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
allantoin metabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
negative regulation of protein phosphorylation	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
negative regulation of endothelial cell proliferation	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
guanine catabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
inosine catabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
deoxyinosine catabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
adenosine catabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
deoxyadenosine catabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
deoxyguanosine catabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
AMP catabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
IMP catabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
activation of cysteine-type endopeptidase activity involved in apoptotic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
lactation	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
hypoxanthine catabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
xanthine catabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
negative regulation of gene expression	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
iron-sulfur cluster assembly	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
amide catabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
negative regulation of endothelial cell differentiation	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
GMP catabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
dGMP catabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
dAMP catabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
negative regulation of phosphatidylinositol 3-kinase/protein kinase B signal transduction	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
positive regulation of p38MAPK cascade	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
negative regulation of vascular endothelial growth factor signaling pathway	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
positive regulation of reactive oxygen species metabolic process	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
negative regulation of vasculogenesis	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
negative regulation of inflammatory response to antigenic stimulus	Guanine nucleotide-binding protein G	Homo sapiens (human)
renal water homeostasis	Guanine nucleotide-binding protein G	Homo sapiens (human)
G protein-coupled receptor signaling pathway	Guanine nucleotide-binding protein G	Homo sapiens (human)
regulation of insulin secretion	Guanine nucleotide-binding protein G	Homo sapiens (human)
cellular response to glucagon stimulus	Guanine nucleotide-binding protein G	Homo sapiens (human)
negative regulation of protein phosphorylation	TAR DNA-binding protein 43	Homo sapiens (human)
mRNA processing	TAR DNA-binding protein 43	Homo sapiens (human)
RNA splicing	TAR DNA-binding protein 43	Homo sapiens (human)
negative regulation of gene expression	TAR DNA-binding protein 43	Homo sapiens (human)
regulation of protein stability	TAR DNA-binding protein 43	Homo sapiens (human)
positive regulation of insulin secretion	TAR DNA-binding protein 43	Homo sapiens (human)
response to endoplasmic reticulum stress	TAR DNA-binding protein 43	Homo sapiens (human)
positive regulation of protein import into nucleus	TAR DNA-binding protein 43	Homo sapiens (human)
regulation of circadian rhythm	TAR DNA-binding protein 43	Homo sapiens (human)
regulation of apoptotic process	TAR DNA-binding protein 43	Homo sapiens (human)
negative regulation by host of viral transcription	TAR DNA-binding protein 43	Homo sapiens (human)
rhythmic process	TAR DNA-binding protein 43	Homo sapiens (human)
regulation of cell cycle	TAR DNA-binding protein 43	Homo sapiens (human)
3'-UTR-mediated mRNA destabilization	TAR DNA-binding protein 43	Homo sapiens (human)
3'-UTR-mediated mRNA stabilization	TAR DNA-binding protein 43	Homo sapiens (human)
nuclear inner membrane organization	TAR DNA-binding protein 43	Homo sapiens (human)
amyloid fibril formation	TAR DNA-binding protein 43	Homo sapiens (human)
regulation of gene expression	TAR DNA-binding protein 43	Homo sapiens (human)
phosphatidylinositol biosynthetic process	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
phosphatidylinositol phosphate biosynthetic process	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
endosome organization	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
Golgi organization	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
phosphatidylinositol biosynthetic process	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
phosphatidylinositol phosphate biosynthetic process	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
endosome organization	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
Golgi organization	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
lysosome organization	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
phosphatidylinositol biosynthetic process	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
receptor-mediated endocytosis	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
signal transduction	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
inner ear development	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
phosphatidylinositol phosphate biosynthetic process	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
phosphatidylinositol-mediated signaling	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
1-phosphatidylinositol 4-kinase activity	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
protein binding	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
ATP binding	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
kinase activity	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
cadherin binding	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
xanthine dehydrogenase activity	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
xanthine oxidase activity	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
iron ion binding	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
protein binding	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
protein homodimerization activity	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
molybdopterin cofactor binding	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
flavin adenine dinucleotide binding	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
2 iron, 2 sulfur cluster binding	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
hypoxanthine dehydrogenase activity	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
hypoxanthine oxidase activity	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
FAD binding	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
G protein activity	Guanine nucleotide-binding protein G	Homo sapiens (human)
adenylate cyclase activator activity	Guanine nucleotide-binding protein G	Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA binding	TAR DNA-binding protein 43	Homo sapiens (human)
DNA binding	TAR DNA-binding protein 43	Homo sapiens (human)
double-stranded DNA binding	TAR DNA-binding protein 43	Homo sapiens (human)
RNA binding	TAR DNA-binding protein 43	Homo sapiens (human)
mRNA 3'-UTR binding	TAR DNA-binding protein 43	Homo sapiens (human)
protein binding	TAR DNA-binding protein 43	Homo sapiens (human)
lipid binding	TAR DNA-binding protein 43	Homo sapiens (human)
identical protein binding	TAR DNA-binding protein 43	Homo sapiens (human)
pre-mRNA intronic binding	TAR DNA-binding protein 43	Homo sapiens (human)
molecular condensate scaffold activity	TAR DNA-binding protein 43	Homo sapiens (human)
1-phosphatidylinositol 4-kinase activity	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
ATP binding	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
magnesium ion binding	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
1-phosphatidylinositol 4-kinase activity	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
protein binding	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
ATP binding	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
AP-3 adaptor complex binding	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
1-phosphatidylinositol 4-kinase activity	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
protein binding	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
ATP binding	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
14-3-3 protein binding	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
cytoplasm	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
cytosol	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
plasma membrane	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
focal adhesion	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
membrane	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
Golgi-associated vesicle membrane	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
extracellular exosome	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
plasma membrane	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
cytoplasm	Phosphatidylinositol 4-kinase alpha	Homo sapiens (human)
cytosol	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
extracellular space	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
peroxisome	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
cytosol	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
sarcoplasmic reticulum	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
extracellular space	Xanthine dehydrogenase/oxidase	Homo sapiens (human)
plasma membrane	Guanine nucleotide-binding protein G	Homo sapiens (human)
intracellular non-membrane-bounded organelle	TAR DNA-binding protein 43	Homo sapiens (human)
nucleus	TAR DNA-binding protein 43	Homo sapiens (human)
nucleoplasm	TAR DNA-binding protein 43	Homo sapiens (human)
perichromatin fibrils	TAR DNA-binding protein 43	Homo sapiens (human)
mitochondrion	TAR DNA-binding protein 43	Homo sapiens (human)
cytoplasmic stress granule	TAR DNA-binding protein 43	Homo sapiens (human)
nuclear speck	TAR DNA-binding protein 43	Homo sapiens (human)
interchromatin granule	TAR DNA-binding protein 43	Homo sapiens (human)
nucleoplasm	TAR DNA-binding protein 43	Homo sapiens (human)
chromatin	TAR DNA-binding protein 43	Homo sapiens (human)
Golgi membrane	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
endoplasmic reticulum membrane	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
cytosol	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
plasma membrane	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
membrane	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
early endosome membrane	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
endosome	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
trans-Golgi network	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
plasma membrane	Phosphatidylinositol 4-kinase type 2-beta	Homo sapiens (human)
BLOC-1 complex	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
Golgi membrane	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
mitochondrion	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
lysosomal membrane	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
endosome	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
cytosol	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
plasma membrane	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
membrane	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
dendrite	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
cytoplasmic vesicle	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
early endosome membrane	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
growing cell tip	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
presynaptic membrane	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
neuron projection	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
neuronal cell body	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
perikaryon	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
membrane raft	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
trans-Golgi network	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
plasma membrane	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
endosome	Phosphatidylinositol 4-kinase type 2-alpha	Homo sapiens (human)
Golgi membrane	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
mitochondrial outer membrane	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
endosome	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
Golgi apparatus	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
cytosol	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
rough endoplasmic reticulum membrane	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
perinuclear region of cytoplasm	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
membrane	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
cytoplasm	Phosphatidylinositol 4-kinase beta	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Assay ID	Title	Year	Journal	Article
AID1745845	Primary qHTS for Inhibitors of ATXN expression
AID588497	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set	2006	Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5	Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588497	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID651635	Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID588499	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set	2006	Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5	Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588499	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504812	Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign	2010	Endocrinology, Jul, Volume: 151, Issue:7	A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID588501	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set	2006	Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5	Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588501	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504810	Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign	2010	Endocrinology, Jul, Volume: 151, Issue:7	A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID1347154	Primary screen GU AMC qHTS for Zika virus inhibitors	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1508630	Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay	2021	Cell reports, 04-27, Volume: 35, Issue:4	A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1324539	Cytotoxicity against African green monkey Vero cells incubated for 24 hrs by neutral red uptake assay	2016	Journal of medicinal chemistry, 12-08, Volume: 59, Issue:23	In Silico Discovery and Validation of Amide Based Small Molecule Targeting the Enzymatic Site of Shiga Toxin.
AID155650	Inhibitory activity (IC50) against human phosphatidylinositol 4-kinase at the ATP binding site	1990	Journal of medicinal chemistry, Aug, Volume: 33, Issue:8	Purine derivatives as competitive inhibitors of human erythrocyte membrane phosphatidylinositol 4-kinase.
AID155653	Binding affinity (Ki) against human phosphatidylinositol 4-kinase	1990	Journal of medicinal chemistry, Aug, Volume: 33, Issue:8	Purine derivatives as competitive inhibitors of human erythrocyte membrane phosphatidylinositol 4-kinase.
AID1452128	Inhibition of ATPgammaS-BODIPY binding to Thermotoga maritima His-tagged HK853 expressed in Escherichia coli BL21(DE3)pLysS Rosetta preincubated for 30 mins prior to ATPgammaS-BODIPY addition measured after 1 hr by coomassie staining-based SDS-PAGE analys	2017	Journal of medicinal chemistry, 10-12, Volume: 60, Issue:19	Rational Design of Selective Adenine-Based Scaffolds for Inactivation of Bacterial Histidine Kinases.
AID274559	Inhibition of Toxoplasma gondii 6 oxopurine phosphoribosyl transferase	2006	Journal of medicinal chemistry, Dec-14, Volume: 49, Issue:25	Lead compounds for antimalarial chemotherapy: purine base analogs discriminate between human and P. falciparum 6-oxopurine phosphoribosyltransferases.
AID1254099	Binding affinity to rabbit muscle glycogen phosphorylase by STD NMR spectrometric analysis	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Ligand-Orientation Based Fragment Selection in STD NMR Screening.
AID287937	Inhibition of human xanthine oxidase	2007	Bioorganic & medicinal chemistry, May-15, Volume: 15, Issue:10	The screening and characterization of 6-aminopurine-based xanthine oxidase inhibitors.
AID1437510	Inhibition of human GST-tagged CDK2/bovine His-tagged Cyclin A at 100 uM relative to untreated control	2017	Journal of medicinal chemistry, 03-09, Volume: 60, Issue:5	Cyclin-Dependent Kinase (CDK) Inhibitors: Structure-Activity Relationships and Insights into the CDK-2 Selectivity of 6-Substituted 2-Arylaminopurines.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Timeframe	Studies, This Drug (%)	All Drugs %
pre-1990	177 (13.10)	18.7374
1990's	329 (24.35)	18.2507
2000's	516 (38.19)	29.6817
2010's	293 (21.69)	24.3611
2020's	36 (2.66)	2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Publication Type	This drug (%)	All Drugs (%)
Trials	90 (6.39%)	5.53%
Reviews	162 (11.50%)	6.00%
Case Studies	97 (6.88%)	4.05%
Observational	0 (0.00%)	0.25%
Other	1,060 (75.23%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (16)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
A Phase 2 Study of Blinatumomab (NSC# 765986) in Combination With Nivolumab (NSC # 748726), a Checkpoint Inhibitor of PD-1, in B-ALL Patients Aged >/= 1 to < 31 Years Old With First Relapse [NCT04546399]	Phase 2	550 participants (Anticipated)	Interventional	2020-12-04	Suspended(stopped due to Other - FDA Partial Clinical Hold)
A Phase III Randomized Trial Investigating Bortezomib (NSC# 681239) on a Modified Augmented BFM (ABFM) Backbone in Newly Diagnosed T-Lymphoblastic Leukemia (T-ALL) and T-Lymphoblastic Lymphoma (T-LLy) [NCT02112916]	Phase 3	847 participants (Actual)	Interventional	2014-10-04	Active, not recruiting
International Phase 3 Trial in Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia (Ph+ALL) Testing Imatinib in Combination With Two Different Cytotoxic Chemotherapy Backbones [NCT03007147]	Phase 3	475 participants (Anticipated)	Interventional	2017-08-08	Recruiting
Risk-Stratified Randomized Phase III Testing of Blinatumomab (NSC#765986) in First Relapse of Childhood B-Lymphoblastic Leukemia (B-ALL) [NCT02101853]	Phase 3	669 participants (Actual)	Interventional	2014-12-17	Active, not recruiting
Intensified Methotrexate, Nelarabine (Compound 506U78) and Augmented BFM Therapy for Children and Young Adults With Newly Diagnosed T-cell Acute Lymphoblastic Leukemia (ALL) or T-cell Lymphoblastic Lymphoma [NCT00408005]	Phase 3	1,895 participants (Actual)	Interventional	2007-01-22	Active, not recruiting
High Risk B-Precursor Acute Lymphoblastic Leukemia (ALL) [NCT00075725]	Phase 3	3,154 participants (Actual)	Interventional	2003-12-29	Completed
Standard Risk B-precursor Acute Lymphoblastic Leukemia (ALL) [NCT00103285]	Phase 3	5,377 participants (Actual)	Interventional	2005-04-11	Completed
A Phase 3 Trial Investigating Blinatumomab (NSC# 765986) in Combination With Chemotherapy in Patients With Newly Diagnosed Standard Risk or Down Syndrome B-Lymphoblastic Leukemia (B-ALL) and the Treatment of Patients With Localized B-Lymphoblastic Lymphom [NCT03914625]	Phase 3	6,720 participants (Anticipated)	Interventional	2019-07-03	Recruiting
Risk-Stratified Therapy for Acute Myeloid Leukemia in Down Syndrome [NCT02521493]	Phase 3	312 participants (Anticipated)	Interventional	2015-12-23	Active, not recruiting
A Pilot Study of Intravenous EZN-2285 (SC-PEG E. Coli L-asparaginase) or Intravenous Oncaspar® in the Treatment of Patients With High-Risk Acute Lymphoblastic Leukemia (ALL) [NCT00671034]	Phase 3	166 participants (Actual)	Interventional	2008-07-21	Completed
Treatment of Patients With Newly Diagnosed Standard Risk B-Lymphoblastic Leukemia (B-ALL) or Localized B-Lineage Lymphoblastic Lymphoma (B-LLy) [NCT01190930]	Phase 3	9,350 participants (Actual)	Interventional	2010-08-09	Active, not recruiting
Intensified PEG-Asparaginase in High Risk Acute Lymphoblastic Leukemia (ALL): A Pilot Study [NCT00866307]	Phase 1	104 participants (Actual)	Interventional	2009-02-23	Completed
A Groupwide Pilot Study to Test the Tolerability and Biologic Activity of the Addition of Azacitidine (NSC# 102816) to Chemotherapy in Infants With Acute Lymphoblastic Leukemia (ALL) and KMT2A (MLL) Gene Rearrangement [NCT02828358]	Phase 2	78 participants (Actual)	Interventional	2017-04-01	Active, not recruiting
A Phase III Randomized Trial for Newly Diagnosed High Risk B-Lymphoblastic Leukemia (B-ALL) Including a Stratum Evaluating Dasatinib (NSC#732517) in Patients With Ph-like Tyrosine Kinase Inhibitor (TKI) Sensitive Mutations [NCT02883049]	Phase 3	5,937 participants (Actual)	Interventional	2012-02-29	Active, not recruiting
A Randomized International Phase 3 Trial of Imatinib and Chemotherapy With or Without Blinatumomab in Patients With Newly-Diagnosed Philadelphia Chromosome-Positive or Philadelphia Chromosome-Like ABL-Class B-Cell Acute Lymphoblastic Leukemia [NCT06124157]	Phase 3	680 participants (Anticipated)	Interventional	2024-01-22	Not yet recruiting
A Phase 3 Randomized Trial of Inotuzumab Ozogamicin (NSC#: 772518) for Newly Diagnosed High-Risk B-ALL; Risk-Adapted Post-Induction Therapy for High-Risk B-ALL, Mixed Phenotype Acute Leukemia, and Disseminated B-LLy [NCT03959085]	Phase 3	4,772 participants (Anticipated)	Interventional	2019-10-31	Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT00075725 (7) [back to overview]	Correlation of Minimal Residual Disease (MRD) Negative With Overall Survival (OS).
NCT00075725 (7) [back to overview]	Correlation of Early Marrow Response Status With MRD Negative.
NCT00075725 (7) [back to overview]	Correlation of Early Marrow Response Status With MRD Positive.
NCT00075725 (7) [back to overview]	Correlation of Minimal Residual Disease (MRD) Negative With Event Free Survival (EFS).
NCT00075725 (7) [back to overview]	Correlation of Minimal Residual Disease (MRD) Positive With Event Free Survival (EFS)
NCT00075725 (7) [back to overview]	Correlation of Minimal Residual Disease (MRD) Positive With Overall Survival (OS)
NCT00075725 (7) [back to overview]	Comparison of the Increase in Cure Rate of High Risk ALL Without Causing More Serious Side Effects Between Interventions
NCT00103285 (10) [back to overview]	Early Marrow Status (EMS) by MRD Status End Induction (Day 29)
NCT00103285 (10) [back to overview]	Event-Free Survival (EFS) for Low MRD (Negative) Subjects by Genetic Subset (TEL/Trisomy Positive vs Negative)
NCT00103285 (10) [back to overview]	Event-free Survival (EFS) for SR-High Patients.
NCT00103285 (10) [back to overview]	Event-free Survival (EFS) for SR-Low Patients
NCT00103285 (10) [back to overview]	Event-Free Survival Probability According to MRD Status End Induction (Day 29)
NCT00103285 (10) [back to overview]	Overall Survival Probability (OS) According to Induction Day 29 MRD Status
NCT00103285 (10) [back to overview]	Event-free Survival (EFS) for SR-Average ALL Patients
NCT00103285 (10) [back to overview]	Event-free Survival (EFS) for SR-Average ALL Patients
NCT00103285 (10) [back to overview]	Health-related Quality of Life Relative to Physical, Social and Emotional Impairment
NCT00103285 (10) [back to overview]	Optimal Time Point for Advance Health Related Quality of Life Intervention
NCT00408005 (8) [back to overview]	Disease-free Survival (DFS) for Randomized Methotrexate T-ALL Cohort (Arm I + Arm II vs. Arm III + Arm IV)
NCT00408005 (8) [back to overview]	Disease-free Survival (DFS) for Randomized Methotrexate T-ALL Cohort (Arm I vs. Arm II vs. Arm III vs. Arm IV)
NCT00408005 (8) [back to overview]	Disease-free Survival (DFS) for Randomized Nelarabine T-ALL Cohort (Arm I + Arm III vs. Arm II + Arm IV)
NCT00408005 (8) [back to overview]	Disease-free Survival (DFS) for Randomized Nelarabine T-ALL Cohort (Arm I vs. Arm II vs. Arm III vs. Arm IV)
NCT00408005 (8) [back to overview]	Cumulative Incidence of CNS Relapse for T-ALL by Risk Group
NCT00408005 (8) [back to overview]	Cumulative Incidence of CNS Relapse for T-ALL by Risk Group
NCT00408005 (8) [back to overview]	Disease-free Survival (DFS) for T-cell Lymphoblastic Lymphoma (T-LLy) Cohort
NCT00408005 (8) [back to overview]	Disease-free Survival (DFS) for T-cell Lymphoblastic Lymphoma (T-LLy) Cohort
NCT00671034 (9) [back to overview]	Percentage of Participants With Complete Remission at the End of Induction
NCT00671034 (9) [back to overview]	Percentage of Participants With Event-free Survival (EFS)
NCT00671034 (9) [back to overview]	Percentage of Participants With Minimal Residual Disease (MRD)<0.01% at the End of Induction
NCT00671034 (9) [back to overview]	Asparaginase Level
NCT00671034 (9) [back to overview]	Pharmacodynamics (PD)
NCT00671034 (9) [back to overview]	Pharmacokinetics (PK) (Half-life of SC-PEG E. Coli L-asparaginase (EZN-2285) Compared to Pegaspargase During Induction and Consolidation Therapy)
NCT00671034 (9) [back to overview]	Plasma and CSF Concentrations of Asparagine in ug/ml
NCT00671034 (9) [back to overview]	Toxicities During Post Induction Intensification Therapy (All Grades)
NCT00671034 (9) [back to overview]	Immunogenicity
NCT00866307 (2) [back to overview]	AALL08P1 Safety Outcome
NCT00866307 (2) [back to overview]	AALL08P1 Feasibility Outcome
NCT01190930 (41) [back to overview]	Characterize Vincristine-associated Neuropathy in Children Undergoing Therapy for Average Risk (AR) ALL by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 7 (Boys)/End of Therapy (Girls): Right
NCT01190930 (41) [back to overview]	DFS for SR Down Syndrome Patients With Standardized Treatment and Enhanced Supportive Care
NCT01190930 (41) [back to overview]	DFS in Average Risk (AR) Patients Based on the Pulse Frequency Randomization
NCT01190930 (41) [back to overview]	DFS in Low Risk (LR) Patients Based on Randomization to 1 of 2 Low-intensity Regimens
NCT01190930 (41) [back to overview]	Disease Free Survival (DFS) in Average Risk (AR) Patients Based on the Methotrexate Dose Randomization
NCT01190930 (41) [back to overview]	Event Free Survival (EFS) for B-LLy Patients
NCT01190930 (41) [back to overview]	Overall Survival (OS) for B-LLy Patients
NCT01190930 (41) [back to overview]	Sample Collection of Central Path Review Slides in B-LLy Patients
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 4: Emotional
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 4: Physical
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 4: Social Functioning
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 7 (Boys)/End of Therapy (Girls): Emotional
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 7 (Boys)/End of Therapy (Girls): Physical
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 7 (Boys)/End of Therapy (Girls): Social Functioning
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients Overall at End of Consolidation Therapy: Emotional
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients Overall at End of Consolidation Therapy: Physical
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients Overall at End of Consolidation Therapy: Social Functioning
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients Overall at End of Maintenance Cycle 1: Emotional
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients Overall at End of Maintenance Cycle 1: Physical
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients Overall at End of Maintenance Cycle 1: Social Functioning
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients Overall at End of Maintenance Cycle 4: Emotional
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients Overall at End of Maintenance Cycle 4: Physical
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients Overall at End of Maintenance Cycle 4: Social Functioning
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients Overall at End of Maintenance Cycle 7 (Boys)/End of Therapy (Girls): Emotional
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients Overall at End of Maintenance Cycle 7 (Boys)/End of Therapy (Girls): Physical
NCT01190930 (41) [back to overview]	Burden of Therapy in AR Patients Overall at End of Maintenance Cycle 7 (Boys)/End of Therapy (Girls): Social Functioning
NCT01190930 (41) [back to overview]	Burden of Therapy in Boy AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Therapy: Emotional
NCT01190930 (41) [back to overview]	Burden of Therapy in Boy AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Therapy: Physical
NCT01190930 (41) [back to overview]	Burden of Therapy in Boy AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Therapy: Social Functioning
NCT01190930 (41) [back to overview]	Burden of Therapy in Boy AR Patients Overall at End of Therapy: Emotional
NCT01190930 (41) [back to overview]	Burden of Therapy in Boy AR Patients Overall at End of Therapy: Physical
NCT01190930 (41) [back to overview]	Burden of Therapy in Boy AR Patients Overall at End of Therapy: Social Functioning
NCT01190930 (41) [back to overview]	Characterize Vincristine-associated Neuropathy in Children Undergoing Therapy for Average Risk (AR) ALL 12 Months Post Therapy: Left
NCT01190930 (41) [back to overview]	Characterize Vincristine-associated Neuropathy in Children Undergoing Therapy for Average Risk (AR) ALL 12 Months Post Therapy: Right
NCT01190930 (41) [back to overview]	Characterize Vincristine-associated Neuropathy in Children Undergoing Therapy for Average Risk (AR) ALL at End of Consolidation Therapy-Left
NCT01190930 (41) [back to overview]	Characterize Vincristine-associated Neuropathy in Children Undergoing Therapy for Average Risk (AR) ALL at End of Consolidation Therapy-Right
NCT01190930 (41) [back to overview]	Characterize Vincristine-associated Neuropathy in Children Undergoing Therapy for Average Risk (AR) ALL at End of Maintenance Cycle 1: Left
NCT01190930 (41) [back to overview]	Characterize Vincristine-associated Neuropathy in Children Undergoing Therapy for Average Risk (AR) ALL at End of Maintenance Cycle 1: Right
NCT01190930 (41) [back to overview]	Characterize Vincristine-associated Neuropathy in Children Undergoing Therapy for Average Risk (AR) ALL at End of Maintenance Cycle 7 (Boys)/End of Therapy (Girls): Left
NCT01190930 (41) [back to overview]	Characterize Vincristine-associated Neuropathy in Children Undergoing Therapy for Average Risk (AR) ALL at End of Maintenance Cycle 7 (Boys)/End of Therapy (Girls): Right
NCT01190930 (41) [back to overview]	Characterize Vincristine-associated Neuropathy in Children Undergoing Therapy for Average Risk (AR) ALL by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 7 (Boys)/End of Therapy (Girls): Left
NCT02101853 (4) [back to overview]	Disease Free Survival (DFS) of High-risk (HR) and Intermediate-risk (IR) Relapse Patients
NCT02101853 (4) [back to overview]	Disease Free Survival (DFS) of Low Risk (LR) Relapse Patients
NCT02101853 (4) [back to overview]	Overall Survival (OS) of HR and IR Relapse Patients
NCT02101853 (4) [back to overview]	Overall Survival (OS) of LR Relapse Patients
NCT02112916 (6) [back to overview]	EFS for Very High Risk (VHR) T-ALL Patients Treated With High Risk (HR) Berlin-Frankfurt-Munster (BFM) Intensification Blocks Who Become Minimal Residual Disease (MRD) Negative and Those Who Remain MRD Positive at the End of HR Block 3
NCT02112916 (6) [back to overview]	EFS for Very High Risk (VHR) T-LLy Patients Treated With HR Berlin-Frankfurt-Munster (BFM) Intensification Blocks Who Have Complete or Partial Remission and Those Who do Not Respond
NCT02112916 (6) [back to overview]	Event-free Survival (EFS) for Modified Augmented Berlin-Frankfurt-Munster Backbone With or Without Bortezomib in All Randomized Patients
NCT02112916 (6) [back to overview]	Toxicity Rates Associated With Modified Standard Therapy, Including Dexamethasone and Additional Pegaspargase
NCT02112916 (6) [back to overview]	Cumulative Incidence Rates of Isolated Central Nervous System (CNS) Relapse for SR and IR T-ALL Patients on the Non-bortezomib Containing Arm on This Study (no CRT) and Similar Patients on AALL0434 (Receive CRT)
NCT02112916 (6) [back to overview]	EFS for Standard (SR) and Intermediate Risk (IR) T-ALL Patients on the Non-bortezomib Containing Arm on This Study (no Cranial Radiation Therapy [CRT]) and Similar Patients on AALL0434 (Received CRT)
NCT02828358 (5) [back to overview]	Biologic Activity, Defined as Global Deoxyribonucleic Acid (DNA) Methylation Change in Peripheral Blood Mononuclear Cells (PBMC)s; Day 1 Prior to First Course of Azacitidine
NCT02828358 (5) [back to overview]	Biologic Activity, Defined as Global Deoxyribonucleic Acid (DNA) Methylation Change in Peripheral Blood Mononuclear Cells (PBMC)s; Day 1 Prior to Second Course of Azacitidine
NCT02828358 (5) [back to overview]	Biologic Activity, Defined as Global Deoxyribonucleic Acid (DNA) Methylation Change in Peripheral Blood Mononuclear Cells (PBMC)s; Day 5 of First Course of Azacitidine
NCT02828358 (5) [back to overview]	Biologic Activity, Defined as Global Deoxyribonucleic Acid (DNA) Methylation Change in Peripheral Blood Mononuclear Cells (PBMC)s; Day 5 of Second Course of Azacitidine
NCT02828358 (5) [back to overview]	Tolerability of Azacitidine in Combination With Interfant-06 Standard Chemotherapy in Evaluable Infant Patients With Newly Diagnosed ALL With KMT2A Gene Rearrangement (KMT2A-R). KMT2A Gene Rearrangement (KMT2A-R)

Correlation of Minimal Residual Disease (MRD) Negative With Overall Survival (OS).

Bone marrow MRD status is defined as negative with < .01 detectable leukemia cells. (NCT00075725)
Timeframe: 5 years

Intervention	percentage of participants (Number)
Dexamethasone and Capizzi Methotrexate Patients < 10 Years	95.4
Dexamethasone, High Dose Methotrexate (Non Randomly Assigned)	92.9
Dexamethasone & Capizzi Methotrexate Patients => 10 Years Old	87.4
Dexamethasone, High Dose Methotrexate (IM) < 10 Years	98.1
Prednisone, Capizzi Methotrexate <10 Years	93.3
Prednisone, Capizzi Methotrexate >= 10 Years	90.2
Prednisone and High Dose Methotrexate < 10 Yrs Old	94.5
Prednisone and High Dose Methotrexate >=10 Years	90.5
Dexamethasone, High Dose Methotrexate (IM) >= 10 Years	91.6
Prednisone, Capizzi Methotrexate (Down's Syndrome)	78.3
Dexamethasone, Capizzi Methotrexate Down Syndrome (Non Random)	25.0

Intervention	percentage of participants (Number)
Dexamethasone and Capizzi Methotrexate Patients < 10 Years	86.4
Dexamethasone, High Dose Methotrexate (Non Randomly Assigned)	93.6
Dexamethasone & Capizzi Methotrexate Patients => 10 Years Old	80.5
Dexamethasone, High Dose Methotrexate (IM) < 10 Years	93.1
Prednisone, Capizzi Methotrexate <10 Years	86.5
Prednisone, Capezzi Methotrexate >= 10 Years	83.4
Prednisone and High Dose Methotrexate < 10 Yrs Old	84.2
Prednisone and High Dose Methotrexate >=10 Years	83.9
Dexamethasone, High Dose Methotrexate (IM) >= 10 Years	85.3
Prednisone, Capezzi Methotrexate (Down's Syndrome)	74.4
Dexamethasone, Capizzi Methotrexate Down Syndrome (Non Random)	25

Intervention	percentage of participants (Number)
Dexamethasone and Capizzi Methotrexate Patients < 10 Years	66.5
Dexamethasone, High Dose Methotrexate (Non Randomly Assigned)	43.3
Dexamethasone & Capizzi Methotrexate Patients => 10 Years Old	35.4
Dexamethasone, High Dose Methotrexate (IM) < 10 Years	80
Prednisone, Capizzi Methotrexate <10 Years	34.7
Prednisone, Capizzi Methotrexate >= 10 Years	39
Prednisone and High Dose Methotrexate < 10 Yrs Old	55
Prednisone and High Dose Methotrexate >=10 Years	47.8
Dexamethasone, High Dose Methotrexate (IM) >= 10 Years	49.4

Intervention	percentage of participants (Number)
Dexamethasone and Capizzi Methotrexate Patients < 10 Years	79.2
Dexamethasone, High Dose Methotrexate (Non Randomly Assigned)	69.9
Dexamethasone & Capizzi Methotrexate Patients => 10 Years Old	65.6
Dexamethasone, High Dose Methotrexate (IM) < 10 Years	86.2
Prednisone, Capizzi Methotrexate <10 Years	93.8
Prednisone, Capizzi Methotrexate >= 10 Years	63.1
Predisone and High Dose Methotrexate < 10 Yrs Old	84.2
Prednisone and High Dose Methotrexate >=10 Years	73.6
Dexamethasone, High Dose Methotrexate (IM) >= 10 Years	74.6

Intervention	percentage of participants (Number)
Dexamethasone and Capizzi Methotrexate Patients < 10 Years	83.2
Dexamethasone, High Dose Methotrexate (Non Randomly Assigned)	81.6
Dexamethasone & Capizzi Methotrexate Patients => 10 Years Old	69.1
Dexamethasone, High Dose Methotrexate (IM) < 10 Years	91.2
Prednisone, Capizzi Methotrexate <10 Years	82.1
Prednisone, Capezzi Methotrexate >= 10 Years	73.5
Predisone and High Dose Methotrexate < 10 Yrs Old	80.8
Prenisone and High Dose Methotrexate >=10 Years	75.8
Dexamethasone, High Dose Methotrexate (IM) >= 10 Years	77.0
Prenisone, Capezzi Methotrexate (Down's Syndrome)	61.8
Dexamethasone, Capizzi Methotrexate Down Syndrome (Non Random)	44.4

Intervention	Participants (Count of Participants)
All Patients for Induction, MRD Negative	4378
All Patients for Induction, MRD Positive	258

Intervention	Percent probability (Number)
Group 1-SR-low ALL, Arm I-combination Chemotherapy	95.22
Group 2-SR-avg ALL, Arm I-combination Chemotherapy	88.52

Intervention	Percent probability (Number)
SR-low ALL, Arm I-combination Chemotherapy	95.22
SR-low ALL, Arm II-combination Chemotherapy	93.96

Intervention	Percent Probability (Number)
Induction Therapy, MRD Negative	91.39
Induction Therapy, MRD Positive	79.86

Intervention	percent probability (Number)
Induction Therapy, MRD Negative	97.07
Induction Therapy, MRD Positive	90.47

Intervention	percent probability (Number)
	Standard and Intensified therapy
Group 2-SR-avg ALL, Arm III-combination Chemotherapy	88.34
Group 2-SR-avg ALL, Arm IV-combination Chemotherapy	90.51

Intervention	percent probability (Number)
ARM I and ARM II (Combination Chemotherapy)	91.45
ARM III and ARM IV (Combination Chemotherapy)	85.78

Intervention	percent probability (Number)
ARM I (Combination Chemotherapy)	91.76
ARM II (Combination Chemotherapy)	90.53
ARM III (Combination Chemotherapy)	86.06
ARM IV (Combination Chemotherapy)	84.89

Intervention	percent probability (Number)
	Standard and Intensified therapy	Standard therapy
Group 2-SR-avg ALL, Arm I-combination Chemotherapy	83.82	87.41
Group 2-SR-avg ALL, Arm II-combination Chemotherapy	88.89	88.29

Intervention	Percentage of participants (Number)
	Physical Impairment 1 mth after diagnosis	Physical Impairment 6 mths after diagnosis	Physical Impairment 12 mths after diagnosis	Physical Impairment 3 mths post therapy	Social Impairment 1 mth after diagnosis	Social Impairment 6 mths after diagnosis	Social Impairment 12 mths after diagnosis	Social Impairment 3 mths post-therapy	Emotional Impairment 1 mth after diagnosis	Emotional Impairment 6 mths after diagnosis	Emotional Impairment 12 mths after diagnosis	Emotional Impairment 3 mths post-therapy
Induction Therapy	76.39	42.75	29.41	27.84	43.36	23.66	23.53	25.77	38.89	17.56	13.97	8.25

Intervention	Percentage of participants (Number)
	At 1 month after diagnosis	At 3 months post-therapy
Induction Therapy	25.2	24.0

Intervention	percent probability (Number)
ARM I and ARM III (Combination Chemotherapy)	82.96
ARM II and ARM IV (Combination Chemotherapy)	88.30

Intervention	percent probability (Number)
ARM I (Combination Chemotherapy)	89.01
ARM II (Combination Chemotherapy)	90.53
ARM III (Combination Chemotherapy)	78.07
ARM IV (Combination Chemotherapy)	86.46

Intervention	percent probability (Number)
	Intermediate Risk	High Risk
ARM II (Combination Chemotherapy)	1.08	0
ARM IV (Combination Chemotherapy)	0.85	3.45

Intervention	percent probability (Number)
	Low Risk	Intermediate Risk	High Risk
ARM I (Combination Chemotherapy)	1.85	1.16	3.64
ARM III (Combination Chemotherapy)	1.92	9.1	6.52

Intervention	percent probability (Number)
	High Risk	Induction Failure
ARM II (Combination Chemotherapy)	85.0	100

Intervention	percent probability (Number)
	Standard Risk	High Risk
ARM I (Combination Chemotherapy)	87.4	85.1

Intervention	Percentage of participants (Number)
Arm I (Calaspargase Pegol 2100)	92.4
Arm II (Calaspargase Pegol 2500)	97.6
Arm III (Pegaspargase 2500)	94.1

2-aminopurine

Description

Cross-References

Synonyms (62)

Research Excerpts

Toxicity

Pharmacokinetics

Compound-Compound Interactions

Bioavailability

Dosage Studied

Roles (1)

Drug Classes (2)

Protein Targets (11)

Potency Measurements

Inhibition Measurements

Biological Processes (60)

Molecular Functions (29)

Ceullar Components (38)

Bioassays (23)

Research

Studies (1,351)

Market Indicators

Research Demand Index: 54.23

Study Types

Clinical Trials (16)

Trial Overview

Trial Outcomes

Correlation of Minimal Residual Disease (MRD) Negative With Overall Survival (OS).

Correlation of Early Marrow Response Status With MRD Negative.

Correlation of Early Marrow Response Status With MRD Positive.

Correlation of Minimal Residual Disease (MRD) Negative With Event Free Survival (EFS).

Correlation of Minimal Residual Disease (MRD) Positive With Event Free Survival (EFS)

Correlation of Minimal Residual Disease (MRD) Positive With Overall Survival (OS)

Comparison of the Increase in Cure Rate of High Risk ALL Without Causing More Serious Side Effects Between Interventions

Early Marrow Status (EMS) by MRD Status End Induction (Day 29)

Event-Free Survival (EFS) for Low MRD (Negative) Subjects by Genetic Subset (TEL/Trisomy Positive vs Negative)

Event-free Survival (EFS) for SR-High Patients.

Event-free Survival (EFS) for SR-Low Patients

Event-Free Survival Probability According to MRD Status End Induction (Day 29)

Overall Survival Probability (OS) According to Induction Day 29 MRD Status

Event-free Survival (EFS) for SR-Average ALL Patients

Event-free Survival (EFS) for SR-Average ALL Patients

Health-related Quality of Life Relative to Physical, Social and Emotional Impairment

Optimal Time Point for Advance Health Related Quality of Life Intervention

Disease-free Survival (DFS) for Randomized Methotrexate T-ALL Cohort (Arm I + Arm II vs. Arm III + Arm IV)

Disease-free Survival (DFS) for Randomized Methotrexate T-ALL Cohort (Arm I vs. Arm II vs. Arm III vs. Arm IV)

Disease-free Survival (DFS) for Randomized Nelarabine T-ALL Cohort (Arm I + Arm III vs. Arm II + Arm IV)

Disease-free Survival (DFS) for Randomized Nelarabine T-ALL Cohort (Arm I vs. Arm II vs. Arm III vs. Arm IV)

Cumulative Incidence of CNS Relapse for T-ALL by Risk Group

Cumulative Incidence of CNS Relapse for T-ALL by Risk Group

Disease-free Survival (DFS) for T-cell Lymphoblastic Lymphoma (T-LLy) Cohort

Disease-free Survival (DFS) for T-cell Lymphoblastic Lymphoma (T-LLy) Cohort

Percentage of Participants With Complete Remission at the End of Induction

Percentage of Participants With Event-free Survival (EFS)

Percentage of Participants With Minimal Residual Disease (MRD)<0.01% at the End of Induction

Asparaginase Level

Pharmacodynamics (PD)

Pharmacokinetics (PK) (Half-life of SC-PEG E. Coli L-asparaginase (EZN-2285) Compared to Pegaspargase During Induction and Consolidation Therapy)

Plasma and CSF Concentrations of Asparagine in ug/ml

Toxicities During Post Induction Intensification Therapy (All Grades)

Immunogenicity

AALL08P1 Safety Outcome

AALL08P1 Feasibility Outcome

Characterize Vincristine-associated Neuropathy in Children Undergoing Therapy for Average Risk (AR) ALL by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 7 (Boys)/End of Therapy (Girls): Right

DFS for SR Down Syndrome Patients With Standardized Treatment and Enhanced Supportive Care

DFS in Average Risk (AR) Patients Based on the Pulse Frequency Randomization

DFS in Low Risk (LR) Patients Based on Randomization to 1 of 2 Low-intensity Regimens

Disease Free Survival (DFS) in Average Risk (AR) Patients Based on the Methotrexate Dose Randomization

Event Free Survival (EFS) for B-LLy Patients

Overall Survival (OS) for B-LLy Patients

Sample Collection of Central Path Review Slides in B-LLy Patients

Burden of Therapy in AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 4: Emotional

Burden of Therapy in AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 4: Physical

Burden of Therapy in AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 4: Social Functioning

Burden of Therapy in AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 7 (Boys)/End of Therapy (Girls): Emotional

Burden of Therapy in AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 7 (Boys)/End of Therapy (Girls): Physical

Burden of Therapy in AR Patients by Vincristine Pulse Frequency Randomization Groups (4 Week vs. 12 Week) at End of Maintenance Cycle 7 (Boys)/End of Therapy (Girls): Social Functioning

Burden of Therapy in AR Patients Overall at End of Consolidation Therapy: Emotional

Burden of Therapy in AR Patients Overall at End of Consolidation Therapy: Physical

Burden of Therapy in AR Patients Overall at End of Consolidation Therapy: Social Functioning

Intervention	Percentage of participants (Number)
Arm I (Calaspargase Pegol 2100)	72.35
Arm II (Calaspargase Pegol 2500)	80.8
Arm III (Pegaspargase 2500)	79.34

Intervention	Percentage of participants (Number)
Arm I (Calaspargase Pegol 2100)	65.2
Arm II (Calaspargase Pegol 2500)	81
Arm III (Pegaspargase 2500)	72.5

Intervention	percentage of patients (Number)
	Level at least 0.1 IU/mL day 4	Level at least 0.1 IU/mL day 15	Level at least 0.1 IU/mL day 22	Level at least 0.1 IU/mL day 29	Level at least 0.4 IU/mL day 4	Level at least 0.4 IU/mL day 15	Level at least 0.4 IU/mL day 22	Level at least 0.4 IU/mL day 29
Arm I (Calaspargase Pegol 2100)	0	98.4	98.2	94.9	0	75.8	37.5	13.6
Arm II (Calaspargase Pegol 2500)	0	100	100	95.0	0	95.0	62.5	27.5
Arm III (Pegaspargase 2500)	0	100	95.1	28.6	0	93.0	14.6	0

Intervention	mIU/mL (Median)
	Plasma Asparaginase Concentration- Consolidation	Plasma Asparaginase Concentration- Induction
Arm I (Calaspargase Pegol 2100)	575.9	271.6
Arm II (Calaspargase Pegol 2500)	617.2	339.6
Arm III (Pegaspargase 2500)	562.1	72.8

Intervention	hours (Mean)
	Asparaginase half-life during Consolidation	Asparaginase half-life during Induction
Arm I (Calaspargase Pegol 2100)	415.8	305.1
Arm II ( Calaspargase Pegol 2500)	355.9	321.5
Arm III (Pegaspargase 2500)	117.2	126.9

Intervention	ug/mL (Mean)
	CSF asparagine concentration (ug/mL)	Plasma asparagine concentration (ug/mL)
Arm I (Calaspargase Pegol 2100)	0.2	0.2
Arm II (Calaspargase Pegol 2500)	0.19	0.25
Arm III (Pegaspargase 2500)	0.26	0.83

Intervention	Percentage of participants (Number)
	Alergic Reaction - Consolidation	Alergic Reaction - Delayed Intensification I	Alergic Reaction - Interim Maintenance I	CNS - Consolidation	CNS - Delayed Intensification I	CNS - Interim Maintenance I	Hyperbilirubinemia - Consolidation	Hyperbilirubinemia - Delayed Intensification I	Hyperbilirubinemia - Interim Maintenance I	Hyperglycemia - Consolidation	Hyperglycemia - Delayed Intensification I	Hyperglycemia - Interim Maintenance I	Hyperlipidemia - Consolidation	Hyperlipidemia - Delayed Intensification I	Hyperlipidemia - Interim Maintenance I	% patients w/INR increase - Consolidation	% pts w/INR increase - Delayed Intensification I	% patients w/INR increase - Interim Maintenance I	Pancreatitis - Consolidation	Pancreatitis -Delayed Intensification I	Pancreatitis - Interim Maintenance I	% pts w/prolongation of APT time - Consolidation	% pts w/prolongation APT time -Delayed Intension I	%pts w/prolongation APT time-Interim maintenance I	Thrombosis - Consolidation	Thrombosis - Delayed Intensification I	Thrombosis - Interim Maintenance I
Arm I (Calaspargase Pegol 2100)	20.4	4.4	0.0	0.0	0.0	0.0	53.1	28.9	41.3	44.9	44.4	34.8	2.0	2.2	2.2	6.1	6.7	2.2	10.2	2.2	2.2	8.2	8.9	6.5	0.0	2.2	0.0
Arm II (Calaspargase Pegol 2500)	27.3	0.0	0.0	0.0	3.8	0.0	45.5	38.5	27.6	42.4	61.5	44.8	3.0	0.0	3.4	3.0	3.8	0.0	6.1	7.7	3.4	9.1	26.9	6.9	0.0	0.0	0.0
Arm III (Pegaspargase 2500)	23.3	0.0	2.1	0.0	2.6	0.0	30.2	10.5	33.3	46.5	36.8	33.3	7.0	0.0	2.6	7.0	0.0	2.6	7.0	0.0	2.6	7.0	18.4	7.7	2.3	0.0	0.0

Intervention	Z-Score (Mean)
B-ALL Average Risk: VCR/DEX Pulse Every 4 Weeks	-1.12
B-ALL Average Risk: VCR/DEX Pulse Every 12 Weeks	-0.02

Intervention	percent probability (Number)
B-ALL Average Risk: VCR/DEX Pulse Every 4 Weeks	94.10
B-ALL Average Risk: VCR/DEX Pulse Every 12 Weeks	95.13

Intervention	percent probability (Number)
B-ALL Low Risk Arm I (LR-M)	98.75
B-ALL Low Risk Arm II (LR-C)	98.50