Federal Register / Vol. 77, No. 79 / Tuesday, April 24, 2012 / Notices 24499 

opportunities, please contact Elizabeth 

M. Denholm, Ph.D. at 

denholme@niehs.nih.gov. 

Treatment of Acute and Chronic 

Neurological Disorders Using GLP–1, 

Exendin-4 and Analogs 

Description of Technology: Glucagonlike peptide-1 (GLP–1) and related 

peptides, including exendin-4 and 

liraglutide, are incretin mimetics that 

enhance glucose-dependent insulin 

secretion following food ingestion as a 

regulator of glucose homeostasis. 

Exendin-4 and liraglutide are used 

clinically in the safe and effective 

treatment of type 2 diabetes to enhance 

insulin secretion and maintain a 

euglycemic state. These actions are 

primarily mediated at the level of the 

GLP–1 receptor in the pancreas; 

however, these compounds are known 

to enter the brain where the GLP–1 

receptor also is expressed. 

Researchers at the NIH have 

discovered the novel use of GLP–1 and 

exendin-4 analogs in the treatment of 

acute and chronic neurological 

disorders and neurodegenerative 

diseases. Studies conducted in 

extensive cell culture and in mouse 

models using these analogs have 

demonstrated significant neurotrophic 

and neuroprotective actions in models 

of several disorders, including 

Alzheimer’s disease, Parkinson’s 

disease, Huntington’s disease, ALS, 

stroke, head trauma and peripheral 

neuropathy. These studies have now 

been extensively published and 

independently validated by other 

scientific groups. Furthermore, clinical 

studies are ongoing to evaluate the use 

of GLP–1 receptor agonists for the 

treatment of early Alzheimer’s disease, 

Parkinson’s disease and diabetic 

neuropathy by several groups within the 

US and Europe. 

Potential Commercial Applications: 

Therapeutics for: 

• Neurodegenerative diseases— 

Alzheimer’s, Huntington’s, 

Parkinson’s, ALS 

• Stroke 

• Head trauma (traumatic brain injury) 

• Peripheral neuropathies 

Competitive Advantages: 

• Compounds reduce neuronal cell 

death, amyloid deposition and 

neuroinflammation while promoting 

neurogenesis. 

• Compounds in this class have 

already been shown to be safe and 

effective for other indications. 

• Extensive in vitro and animal data 

are available, and clinical studies are 

ongoing. 

• There are extensive publications in 

the literature, both from the inventors 

and independent groups. 

Development Stage: 

• Pre-clinical 

• Clinical 

• In vitro data available 

• In vivo data available (animal) 

• In vivo data available (human) 

Inventors: Nigel Greig, Harold 

Halloway, Maire Doyle, Josephine Egan 

(all of NIA). 

Publications: 

1. Li Y, et al. Exendin-4 ameliorates 

motor neuron degeneration in 

cellular and animal models of 

amyotrophic lateral sclerosis. PLoS 

One. 2012;7(2):e32008. [PMID 

22384126] 

2. Li Y, et al. Enhancing the GLP–1 

receptor signaling pathway leads to 

proliferation and neuroprotection in 

human neuroblastoma cells. J 

Neurochem. 2010 Jun;113(6):1621– 

1631. [PMID 20374430] 

3. Li Y, et al. GLP–1 receptor 

stimulation reduces amyloid-beta 

peptide accumulation and 

cytotoxicity in cellular and animal 

models of Alzheimer’s disease. J 

Alzheimers Dis. 2010;19(4):1205– 

1219. [PMID 20308787] 

4. Li Y, et al. GLP–1 receptor 

stimulation preserves primary 

cortical and dopaminergic neurons 

in cellular and rodent models of 

stroke and Parkinsonism. Proc Natl 

Acad Sci USA. 2009 Jan 

27;106(4):1285–1290. [PMID 

19164583] 

5. Martin B, et al. Exendin-4 improves 

glycemic control, ameliorates brain 

and pancreatic pathologies and 

extends survival in a mouse model 

of Huntington’s disease. Diabetes. 

2009 Feb;58(2):318–328. 

[PMID:18984744] 

6. Perry T, et al. Evidence of GLP–1- 

mediated neuroprotection in an 

animal model of pyridoxineinduced peripheral sensory 

neuropathy. Exp Neurol. 2007 

Feb;203(2):293–301. [PMID 

17125767] 

7. Perry T, Greig NH. Enhancing central 

nervous system endogenous GLP–1 

receptor pathways for intervention 

in Alzheimer’s disease. Curr 

Alzheimers Res. 2005 Jul;2(3):377– 

385. [PMID 15974903] 

8. Greig NH, et al. New therapeutic 

strategies and drug candidates for 

neurodegenerative diseases: p53 

and TNF-alpha inhibitors, and 

GLP–1 receptor agonists. Ann NY 

Acad Sci. 2004 Dec;1035:290–315. 

[PMID 15681814] 

9. Perry TA, Greig NH. A new 

Alzheimer’s disease interventive 

strategy: GLP–1. Curr Drug Targets. 

2004 Aug;5(6):565–571. [PMID 

15270203] 

Listing of additional related 

publications available upon request. 

Intellectual Property: HHS Reference 

No. E–049–2001/0— 

• U.S. Patent 7,576,050 issued 18 Aug 

2009 

• U.S. Patent Application No. 12/ 

317,042 filed 18 Dec 2008 

• Foreign counterparts in Australia, 

Canada, Europe, India, and Japan 

Licensing Contact: Tara L. Kirby, 

Ph.D.; 301–435–4426; 

tarak@mail.nih.gov. 

Collaborative Research Opportunity: 

The National Institute on Aging, Drug 

Design and Development Section, is 

seeking statements of capability or 

interest from parties interested in 

collaborative research to further 

develop, evaluate or commercialize this 

technology. For collaboration 

opportunities, please contact Vio Conley 

at conleyv@mail.nih.gov. 

Dated: April 18, 2012. 

Richard U. Rodriguez, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. 2012–9776 Filed 4–23–12; 8:45 am] 

BILLING CODE 4140–01–P 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Government-Owned Inventions; 

Availability for Licensing: Mouse 

Models 

AGENCY: National Institutes of Health, 

Public Health Service, HHS. 

ACTION: Notice. 

SUMMARY: The inventions listed below 

are owned by an agency of the U.S. 

Government and are available for 

licensing in the U.S. in accordance with 

35 U.S.C. 207 to achieve expeditious 

commercialization of results of 

federally-funded research and 

development. Foreign patent 

applications are filed on selected 

inventions to extend market coverage 

for companies and may also be available 

for licensing. 

FOR FURTHER INFORMATION CONTACT: 

Licensing information for the 

technologies listed below may be 

obtained by writing to the indicated 

licensing contact at the Office of 

Technology Transfer, National Institutes 

of Health, 6011 Executive Boulevard, 

Suite 325, Rockville, Maryland 20852– 

mstockstill on DSK4VPTVN1PROD with NOTICES

24500 Federal Register / Vol. 77, No. 79 / Tuesday, April 24, 2012 / Notices 

3804; telephone: 301–496–7057; fax: 

301–402–0220. 

Smad4 Knockout (Smad4tm1Cxd) Mouse 

Model for Developmental Biology 

Studies 

Description of Mouse: Smad4 

knockout: Smad4 is essential for 

epiblast proliferation, egg cylinder 

formation and mesoderm induction in 

early embryogenesis. 

The TGF-beta-related superfamily 

plays an important role in multiple 

biological systems including 

embryogenesis. TGF-beta ligands 

activate specific receptors, which 

interact with specific Smad proteins, 

which in turn form a complex with a 

common partner, Smad4, that conveys 

the signal to downstream targets. Exon 

8 of the Smad4 gene was disrupted 

using homologous recombination in 

embryonic stem cells. Exon 8 encodes 

the C-terminal domain of Smad4 that is 

essential for the formation of 

heteromeric complexes with the other 

Smads. Mice heterozygous for the 

Smad4 mutation are phenotypically 

normal. Homozygotes, however, die 

early in embryonic development (day 

E6.5–8.5). Smad4 is required for three 

essential functions in early 

embryogenesis: epiblast proliferation, 

egg cylinder formation, and mesoderm 

induction. 

Potential Commercial Application: 

Study of developmental biology in 

conjunction with compounds. 

Development Status: Pre-clinical. 

Developer of Mouse: Chu-Xia Deng, 

Ph.D. (NIDDK). 

Relevant Publication: Yang X, et al. 

The tumor suppressor SMAD4/DPC4 is 

essential for epiblast proliferation and 

mesoderm induction in mice. Proc Natl 

Acad Sci U S A. 1998 Mar 

31;95(7):3667–72. [PMID 9520423]. 

Intellectual Property: HHS Reference 

No. E–133–1999/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Charlene A. 

Sydnor, Ph.D.; 301–435–4689; 

sydnorc@mail.nih.gov. 

Fgfr4 Knockout Mouse Model for 

Respiratory System Studies 

Description of Mouse: FGFR4 

knockout: Lung alveoli fail to develop 

normally in double mutant with FGFR4 

and FGFR3 knockouts. 

The fibroblast growth factor receptor 

4 (fgfr-4) gene was inactivated by 

targeted disruption and homozygous 

recombination to study its possible role 

in lung development. FGFR–4 is 

expressed in postnatal lung, and FGFR– 

4 null mice have no obvious 

abnormalities. However, mice that are 

doubly homozygous for targeted 

disruptions of FGFR3 and FGFR4 

display novel phenotypes, including 

pronounced dwarfism and lung 

abnormalities. The lungs of the double 

knockout mice are normal at birth, but 

they fail to develop secondary septae 

that delimit alveoli and increase the 

surface area of the lung. Although lung 

function is impaired, the double 

homozygous knockout mice are viable 

but sickly. 

Potential Commercial Application: 

Model for the study of respiratory 

system and potential treatments. 

Development Status: Pre-clinical. 

Developer of Mouse: Chu-Xia Deng, 

Ph.D. (NIDDK). 

Relevant Publication: Weinstein M, et 

al. FGFR–3 and FGFR–4 function 

cooperatively to direct alveogenesis in 

the murine lung. Development. 1998 

Sep;125(18):3615–23. [PMID 9716527]. 

Intellectual Property: HHS Reference 

No. E–125–2000/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Charlene A. 

Sydnor, Ph.D.; 301–435–4689; 

sydnorc@mail.nih.gov. 

M5 Muscarinic Receptor Knockout 

(Chrm5tm1Jwe) Mouse Model for 

Neurological Studies 

Description of Mouse: M5 muscarinic 

receptor knockout: Deficiency of M5Rs 

reduces drug-seeking behavior. 

The five Muscarinic Acetylcholine 

(ACh) receptors are G-protein coupled 

receptors (M1R–M5R). M1R, M3R and 

M5R selectively couple to Gq/G11; M2R 

and M4R selectively couple to Gi/Go. 

M5R knockout mice are viable and 

fertile, and have no major 

morphological abnormalities. 

M5 muscarinic ACh receptors are 

located in the central nervous system 

and may contribute to the cognitiveenhancing effects of ACh. M5R 

knockout mice show deficits in two 

hippocampus-dependent cognitive 

tasks, and exhibit reduced cerebral 

blood flow in the cerebral cortex and 

hippocampus, consistent with the 

observation that M5Rs mediate AChmediated dilation of cerebral blood 

vessels. M5R agonists or agonists for 

mixed M1/M5 receptors may be 

effective in the treatment of Alzheimer’s 

disease and related memory disorders. 

The M5R knockout mutation also 

appears to exert a stabilizing effect on 

sensorimotor gating in intact mice, 

which is decreased in schizophrenia. 

Analysis of M5R knockout mice also has 

shown that the lack of M5Rs reduces 

drug-seeking behavior. 

Potential Commercial Application: 

Mouse model for use in neurological 

studies. 

Development Stage: Pre-clinical. 

Developer of Mouse: Ju ̈rgen Wess, 

Ph.D. (NIDDK). 

Relevant Publication: Yamada M, et 

al. Cholinergic dilation of cerebral blood 

vessels is abolished in M(5) muscarinic 

acetylcholine receptor knockout mice. 

Proc Natl Acad Sci U S A. 2001 Nov 

20;98(24):14096–101. [PMID 11707605]. 

Intellectual Property: HHS Reference 

No. E–110–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Charlene A. 

Sydnor, Ph.D.; 301–435–4689; 

sydnorc@mail.nih.gov. 

Stat5a LoxP/Stat5b LoxP (Stat5a/ 

Stat5btm2Mam) Mouse Model for 

Mammopoietic and Lactogenic 

Signaling Studies 

Description of Mouse: Conditional 

knockout of Stat5a and Stat5b: 

Combined deletion of conserved Stat5a 

and Stat5b in mammary epithelium at 

different times during pregnancy reveal 

multiple distinct functions. 

The signal transducer and activator of 

transcription (STAT) family of 

transcription factors conveys signals 

from membrane receptors to the 

nucleus, where they activate diverse 

genetic programs. Stat5a and Stat5b are 

highly conserved proteins that are 

activated by many cytokines, 

erythropoietin, prolactin and growth 

hormone. Despite their similarities, they 

have many unique functions. Stat5a 

deficiency results in the loss of 

prolactin-dependent mammary gland 

development, but does not affect body 

growth. Inactivation of Stat5b does not 

adversely affect mammary development 

and function, but leads to severe growth 

retardation. To study the effects of 

combined deficiency of Stat 5a and 5b 

before and during pregnancy, loxP was 

added to the ends of a DNA fragment 

that contains the two genes which are 

located within a stretch of 110 kb on 

chromosome 11 in a head to head 

orientation with no other genes between 

them. The loxP-flanked fragment was 

introduced into the genome using 

homologous recombination, and deleted 

using two transgenic lines expressing 

Cre in mammary epithelium at different 

times. Deletion of Stat 5 before 

pregnancy prevents epithelial 

proliferation. Ductal characteristics are 

retained but differentiation into 

secretory alveoli does not occur. When 

deletion of Stat5 occurs late in 

pregnancy after differentiation has 

started, differentiation is halted and 

premature death occurs. 

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Federal Register / Vol. 77, No. 79 / Tuesday, April 24, 2012 / Notices 24501 

Potential Commercial Application: 

Mouse model to study mammopoietic 

and lactogenic signaling. 

Development Stage: Pre-clinical. 

Developer of Mouse: Lothar 

Hennighausen, Ph.D. (NIDDK). 

Relevant Publication: Cui Y, et al. 

Inactivation of Stat5 in mouse mammary 

epithelium during pregnancy reveals 

distinct functions in cell proliferation, 

survival, and differentiation. Mol Cell 

Biol. 2004 Sep;24(18):8037–47. [PMID 

15340066]. 

Intellectual Property: HHS Reference 

No. E–114–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Suryanarayana 

(Sury) Vepa, Ph.D., J.D.; 301–435–5020; 

vepas@mail.nih.gov. 

Stat5a Knockout (Stat5atm1Mam) Mouse 

Model for Mammopoietic and 

Lactogenic Signaling Studies 

Description of Mouse: Stat5a 

Knockout: Stat5a deficiency results in 

the loss of prolactin-dependent 

mammary gland development and 

lactogenesis. 

Prolactin induces mammary gland 

development and lactogenesis. Binding 

of Prolactin to its receptor leads to the 

phosphorylation and activation of STAT 

(signal transducers and activators of 

transcription) proteins. Two Stat 

proteins, Stat5a and Stat5b, are 

expressed in mammary tissues during 

pregnancy. Stat5a null mice developed 

normally, and were indistinguishable 

from hemizygous and wild-type 

littermates in size, weight and fertility. 

Mammary lobulo-alveolar outgrowth 

during pregnancy was reduced and 

females failed to lactate after 

parturition. Stat5b, despite 96% 

similarity to Stat5a, could not 

compensate for the loss of Stat5a. Stat5a 

is the principal and obligate mediator of 

mammopoietic and lactogenic signaling. 

Potential Commercial Application: 

Mouse model to study mammopoietic 

and lactogenic signaling. 

Development Stage: Pre-clinical. 

Developer of Mouse: Lothar 

Hennighausen, Ph.D. (NIDDK). 

Relevant Publication: Liu X, et al. 

Stat5a is mandatory for adult mammary 

gland development and lactogenesis. 

Genes Dev. 1997 Jan 15;11(2):179–86. 

[PMID 9009201]. 

Intellectual Property: HHS Reference 

No. E–116–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Suryanarayana 

(Sury) Vepa, Ph.D., J.D.; 301–435–5020; 

vepas@mail.nih.gov. 

Gs Alpha LoxP (Gnastm1Lsw) Mouse 

Model for Metabolism Studies 

Description of Mouse: Generation of a 

floxed Gnsa gene for the G-protein Gs

alpha (Gsa) for the construction of 

conditional knockout mice. 

The heterotrimeric G protein Gsa 

couples many receptors to adenylyl 

cyclase and is essential for hormonestimulated cAMP generation. Previous 

mouse models with germ-line mutations 

in Gnas, the gene that encodes Gsa had 

limited usefulness in trying to decipher 

the role of Gsa pathways in specific 

tissues since only heterozygotes were 

viable and could be analyzed. Analysis 

was further complicated by the fact that 

Gsa is imprinted expressed in many 

metabolically active tissues. 

Gsa-floxed mice were generated so 

that the metabolic effects of Gsa 

deficiency could be examined in 

specific tissues. Exon1, which is 

specific for Gsa, was surrounded with 

loxP recombination sites. Liver-specific 

knockouts of Gsa were obtained by 

mating the Gsa-floxed mice with 

albumin promoter-Cre-transgenic mice. 

Gsa exon1 was efficiently deleted. These 

mice have been used successfully to 

generate other tissue-specfic Gsa 

knockout mice. 

Potential Commercial Application: 

Mouse model to study metabolism. 

Development Stage: Pre-clinical. 

Developer of Mouse: Lee Weinstein, 

M.D. (NIDDK). 

Relevant Publication: Chen M, et al. 

Increased glucose tolerance and reduced 

adiposity in the absence of fasting 

hypoglycemia in mice with liverspecific Gs alpha deficiency. J Clin 

Invest. 2005 Nov;115(11):3217–27. 

[PMID 16239968]. 

Intellectual Property: HHS Reference 

No. E–117–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Suryanarayana 

(Sury) Vepa, Ph.D., J.D.; 301–435–5020; 

vepas@mail.nih.gov. 

Sirt6 LoxP (Sirt6tm1.1Cxd) Mouse Model 

for Liver Studies 

Description of Mouse: Generation of 

floxed Sirtuin 6 for the construction of 

conditional knockout mice. 

The Sirtuins (Sirt1–7), a family of 

seven proteins related to yeast Sir2, are 

histone deacetylases that regulate many 

critical biological processes including 

genomic stability, adaptation to calorie 

restriction and aging. Mice with a 

targeted disruption of Sirt6 had very 

low levels of blood glucose (and 

paradoxically, low insulin levels) and 

died shortly after weaning. 

Hypoglycemia, attributed to increased 

sensitivity to insulin, was the major 

cause for lethality. 

Because of the post-weaning mortality 

of Sirt6 null mice, liver-specific Sirt6 

conditional knockout mice were 

constructed using Cre-Lox technology to 

study the effects on glucose and lipid 

metabolism. Hepatic-specific Sirt6 

deficient mice exhibited increased 

glycolysis and triglyceride synthesis, 

resulting in the development of fatty 

liver. Sirt6 is a potential therapeutic 

target for treating fatty liver disease, the 

most common cause of liver 

dysfunction. 

Potential Commercial Application: 

Mouse model to study the liver. 

Development Stage: Pre-clinical. 

Developer of Mouse: Chuxia Deng, 

Ph.D. (NIDDK). 

Relevant Publication: Kim HS, et al. 

Hepatic-specific disruption of SIRT6 in 

mice results in fatty liver formation due 

to enhanced glycolysis and triglyceride 

synthesis. Cell Metab. 2010 Sep 

8;12(3):224–36. [PMID 20816089]. 

Intellectual Property: HHS Reference 

No. E–121–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Lauren NguyenAntczak, Ph.D., J.D.; 301–435–4074; 

Lauren.Nguyen-Antczak@nih.gov. 

Sirt1 LoxP (Sirt1tm1Cxd) Mouse Model 

for Metabolism and Hepatology Studies 

Description of Mouse: Generation of 

floxed Sirtuin 1 Exon5–Exon6 for the 

construction of conditional knockout 

mice. 

Sirtuin 1 (Sirt1), a homolog of yeast 

Sir 2, is an NAD-dependent histone and 

protein deacetylase. It has a wide range 

of biological functions, ranging from 

DNA damage repair to effects on glucose 

metabolism. Sirt1 null mice die before 

birth due to chromosomal aberrations 

and impaired DNA damage repair. Sirt1 

is thought to affect energy metabolism, 

but the mechanism remains poorly 

understood. In order to study tissuespecific metabolic effects of Sirt1, floxed 

Sirt1 was constructed so that exons 5 

and 6 would be deleted using the CreLox strategy. In contrast to a previously 

reported deletion of Sirt1 exon4, no 

truncated (and potentially active) Sirt1 

forms were detected when exons 5 and 

6 were deleted. 

Hepatic exon 5–6 null Sirt1 mice were 

generated when Floxed Sirt1 exon 5 and 

6 mice were mated with mice that 

expressed the Cre-recombinase in liver. 

The hepatic exon 5–6 null Sirt1 mice 

developed fatty liver under normal 

feeding conditions. This was 

accompanied by increased expression of 

the carbohydrate responsive element 

binding protein, which is a major 

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24502 Federal Register / Vol. 77, No. 79 / Tuesday, April 24, 2012 / Notices 

regulator of lipid synthesis. Sirt1- 

deficient liver also has an impaired 

insulin response, primarily due to 

reduced phosphorylation of the serinethreonine kinase Akt in the presence of 

insulin. 

Potential Commercial Application: 

Mouse model to study metabolism and 

hepatology. 

Development Stage: Pre-clinical. 

Developer of Mouse: Chuxia Deng, 

Ph.D. (NIDDK). 

Relevant Publications: 

1. Wang RH, et al. Liver steatosis and 

increased ChREBP expression in 

mice carrying a liver specific SIRT1 

null mutation under a normal 

feeding condition. Int J Biol Sci. 

2010 Nov 16;6(7):682–90. [PMID 

21103071]. 

2. Wang RH, et al. Hepatic Sirt1 

deficiency in mice impairs mTorc2/ 

Akt signaling and results in 

hyperglycemia, oxidative damage, 

and insulin resistance. J Clin Invest. 

2011 Nov 1;121(11):4477–90. [PMID 

21965330]. 

Intellectual Property: HHS Reference 

No. E–122–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Lauren NguyenAntczak, Ph.D., J.D.; 301–435–4074; 

Lauren.Nguyen-Antczak@nih.gov. 

Fgfr3 Knockout Mouse Model for 

Developmental Biology Studies 

Description of Mouse: FGFR3 

knockout. Complete knockout of the 

FGFR3 gene, the gene in which 

missense mutants cause short statue 

achondroplasia, fails to restrain cartilage 

growth at the bone growth plate, 

allowing bones to elongate excessively 

but fail to ossify. 

Endochondral ossification is a major 

mode of bone formation. Cartilage 

proliferates, undergoes hypertrophy, 

begins to calcify, undergoes a program 

of cell death, and is replaced by 

osteoblasts. Fibroblast Growth Factor 

Receptor 3 (FGFR3) is expressed in 

cartilage rudiments of a wide variety of 

bones, and dominant missense 

mutations in the human FGFR3 gene 

cause achondroplasia, a common form 

of human dwarfism characterized by 

minimal proliferation of the growth 

plate cartilage in long bones. To 

determine the effect of complete 

absence of FGFR3 on bone development 

in mice, targeted disruption of the 

FGFR3 gene was accomplished by 

homologous recombination in 

embryonic stem cells. Remarkably, the 

vertebral column and long bones of 

FGFR3 null mice were extremely long, 

suggesting that in normal development, 

FGFR3 restrains cartilage promotion and 

limits bone elongation so that the 

endochondral ossification program can 

proceed. Restraint of cartilage growth by 

FGFR3 provides a plausible explanation 

for the role of FGFR3 missense 

mutations in human achondroplastic 

dwarfs. 

Potential Commercial Application: 

Mouse model to study developmental 

biology. 

Development Stage: Pre-clinical. 

Developer of Mouse: Chuxia Deng, 

Ph.D. (NIDDK). 

Relevant Publication: Deng C, et al. 

Fibroblast growth factor receptor 3 is a 

negative regulator of bone growth. Cell. 

1996 Mar 22;84(6):911–21. [PMID 

8601314] 

Intellectual Property: HHS Reference 

No. E–123–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Lauren NguyenAntczak, Ph.D., J.D.; 301–435–4074; 

Lauren.Nguyen-Antczak@nih.gov. 

Fgfr2 Knockout (Fgfr2 tm1Cxd) Mouse 

Model for Developmental Biology 

Studies 

Description of Mouse: FGFR2 

knockout is an embryonic lethal 

mutation and blocks limb bud initiation. 

Fibroblast Growth Factor Receptor 2 

(FGFR2) is a high affinity receptor for 

several members of the FGF family. The 

FGFR2 gene was inactivated by deleting 

the entire immunoglobulin-like domain 

of the receptor which is critical for FGF 

binding and FGFR2 activity. Embryos 

that lack this domain die at E10–11.5 

owing to a failure in chorioallantoic 

fusion or placental formation. The 

deletion also blocks limb bud initiation, 

establishing FGFR2 as the major 

receptor that mediates FGF signals 

during limb induction. 

Potential Commercial Application: 

Mouse model to study developmental 

biology. 

Development Stage: Pre-clinical. 

Developer of Mouse: Chuxia Deng, 

Ph.D. (NIDDK). 

Relevant Publication: Xu X, et al. 

Fibroblast growth factor receptor 2 

(FGFR2)-mediated reciprocal regulation 

loop between FGF8 and FGF10 is 

essential for limb induction. 

Development. 1998 Feb;125(4):753–65. 

[PMID 9435295]. 

Intellectual Property: HHS Reference 

No. E–124–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Lauren NguyenAntczak, Ph.D., J.D.; 301–435–4074; 

Lauren.Nguyen-Antczak@nih.gov. 

Alb-tTA (Tg(Alb1-tTA)3123Lng) Mouse 

Model for Liver Function Studies 

Description of Mouse: Tetracyclineresponsive transcriptional activator 

driven by the liver-specific mouse 

albumin promoter (Alb-tTA). 

The E. Coli tetracycline operon 

regulatory system was used to generate 

a liver-specific transcription activation 

system that was inhibited by 

tetracycline. The transcription activator 

was a fused protein consisting of a 

tetracycline repressor gene (tetR) that 

was only active in the presence of 

tetracycline and a herpes simplex virus 

protein (VP–16) transcription activating 

domain. Transcription was induced 

only in the absence of tetracycline (TetOff). A liver-specific promoter such as 

mouse albumin determined that the 

tetracycline-regulated transcriptional 

activator (tTA) would be expressed 

specifically in liver. To study the effect 

of the transcription activator on a target 

gene (for example, Simian Virus 40 

(SV4) large tumor (T) antigen (TAg)) 

specifically in liver, Alb-tTA mice were 

mated with transgenic mice in which 

the Target gene (TAg) was controlled by 

the E. Coli Tetracycline Operator (TetO). In this example, TAg was expressed 

in hepatocytes in the absence of 

Tetracycline, leading to hepatoma 

formation. When the mice were treated 

with tetracycline, TAg was not 

expressed and hepatomas did not form. 

Potential Commercial Application: 

Mouse model to liver function. 

Development Stage: Pre-clinical. 

Developer of Mouse: T. Jake Liang, 

M.D. (NIDDK). 

Relevant Publication: Manickan E, et 

al. Conditional liver-specific expression 

of simian virus 40 T antigen leads to 

regulatable development of hepatic 

neoplasm in transgenic mice. J Biol 

Chem. 2001 Apr 27;276(17):13989–94. 

[PMID 11278564] 

Intellectual Property: HHS Reference 

No. E–125–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Lauren NguyenAntczak, Ph.D., J.D.; 301–435–4074; 

Lauren.Nguyen-Antczak@nih.gov. 

MUP-tTA Mouse Model for Liver 

Function Studies 

Description of Mouse: Tetracyclineresponsive transcriptional activator 

driven by the liver-specific mouse major 

urinary protein promoter (MUP-tTA). 

The E. Coli tetracycline operon 

regulatory system was used to generate 

a liver-specific transcription activation 

system that was inhibited by 

tetracycline. The transcription activator 

was a fused protein consisting of a 

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Federal Register / Vol. 77, No. 79 / Tuesday, April 24, 2012 / Notices 24503 

tetracycline repressor gene (tetR) that 

was only active in the presence of 

tetracycline and a herpes simplex virus 

protein (VP–16) transcription activating 

domain (Tet-Off). Transcription was 

induced only in the absence of 

tetracycline (Tet-Off). A liver-specific 

promoter such as the mouse major 

urinary protein (MUP) promoter 

determined that the tetracyclineregulated transcriptional activator (tTA) 

would be expressed specifically in liver. 

To study the effect of the transcription 

activator on a target gene (for example, 

beta-galactosidase, LacZ) specifically in 

liver, MUP-tTA mice would be mated 

with transgenic mice in which the TAg 

Target gene was controlled by the E. 

Coli Tetracycline Operator (Tet-O). The 

Tet technology may require a separate 

license. 

Potential Commercial Application: 

Mouse model to study liver function. 

Development Stage: Pre-clinical. 

Developer of Mouse: T. Jake Liang, 

M.D. (NIDDK). 

Relevant Publication: Manickan E, et 

al. Conditional liver-specific expression 

of simian virus 40 T antigen leads to 

regulatable development of hepatic 

neoplasm in transgenic mice. J Biol 

Chem. 2001 Apr 27;276(17):13989–94. 

[PMID 11278564] 

Intellectual Property: HHS Reference 

No. E–126–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Lauren NguyenAntczak, Ph.D., J.D.; 301–435–4074; 

Lauren.Nguyen-Antczak@nih.gov. 

mEpoR Knockout/Tg(hEpoR) Mouse 

Model for Anemia and Renal Function 

Studies 

Description of Mouse: mEpoR¥/ 

¥hEpoR+: The mouse Erythropoietin 

Receptor knockout that contains a 

human Erythropoietin Receptor 

transgene can be used to define the 

potency of recombinant erythropoietin 

preparations used to treat anemia 

associated with chronic kidney disease. 

Erythropoietin, acting by binding to 

Erythropoietin receptors (EpoR) on 

erythroid progenitor cells, is required 

for erythropoiesis. Absence of 

erythropoietin or the EpoR in mice 

interrupts erythropoiesis in the fetal 

liver and results in death at embryonic 

day 13.5. An 80-kb human EpoR 

transgene bred onto a mouse EpoR null 

background (provided by F. Constantini 

of Columbia University) restored 

effective erythropoiesis in the EpoR null 

mouse. Erythropoietin preparations 

made utilizing recombinant DNA 

technology are used in the treatment of 

anemia in chronic kidney disease and 

other critical illnesses. The mouse EpoR 

null mouse containing the human EpoR 

transgene can be used to define the 

potency of erythropoietin preparation in 

humans. 

Potential Commercial Applications: 

Model for study of anemia and renal 

function and possible drug screening. 

Developer of Mouse: Constance 

Noguchi, Ph.D. (NIDDK). 

Relevant Publication: Yu X, et al. The 

human erythropoietin receptor gene 

rescues erythropoiesis and 

developmental defects in the 

erythropoietin receptor null mouse. 

Blood. 2001 Jul 15;98(2):475–7. [PMID 

11435319]. 

Intellectual Property: HHS Reference 

No. E–127–2001/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Jennifer S. Wong; 

301–435–4633; wongje@mail.nih.gov. 

Sirt3 Knockout (Sirt3tm1.1Cxd) Mouse 

Model for Cardiology and Metabolism 

Studies 

Description of Mouse: Sirt3 knockout: 

Sirt3 is a mitochondrial-localized tumor 

suppressor that maintains 

mitochondrial integrity and metabolism 

during stress. Sirt3 is a mitochondrial 

protein that is a member of the Sirtuin 

family of NAD-dependent protein 

deacetylases. Sirt3(¥/¥) mice are 

phenotypically normal, but exhibit 

many proteins whose acetylation is 

increased. They generate more reactive 

oxygen species and are more susceptible 

to mammary tumors than normal mice. 

Sirt3 is inactivated in a large percentage 

of human breast and ovarian cancers, 

suggesting that Sirt3 may be a 

mitochondria-localized tumor 

suppressor by maintaining 

mitochondrial integrity and efficient 

oxidative metabolism. 

Potential Commercial Applications: 

Cardiology, Metabolism. 

Developer of Mouse: Chuxia Deng, 

Ph.D. (NIDDK). 

Relevant Publication: Kim HS, et al. 

SIRT3 is a mitochondria-localized 

tumor suppressor required for 

maintenance of mitochondrial integrity 

and metabolism during stress. Cancer 

Cell. 2010 Jan 19;17(1):41–52. [PMID 

20129246]. 

Intellectual Property: HHS Reference 

No. E–119–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Jennifer S. Wong; 

301–435–4633; wongje@mail.nih.gov. 

Sirt1 Knockout (Sirt1tm1.1Cxd) Mouse 

Model for Oncology and Metabolism 

Studies 

Description of Mouse: Sirt1 knockout: 

Sirt1, a protein deacetylase, is a tumor 

suppressor that promotes genome 

stability and regulates proteins involved 

in energy metabolism. 

Yeast Sir2, a nicotinamide adenine 

dinucleotide (NAD)-dependent protein 

deacetylase, has been implicated in 

chromatin silencing, longevity and 

genome stability. Mammals contain a 

family of related deacetylases, the 

sirtuins, of which 7 have been 

identified. Sirt1 is the closest 

mammalian orthologue of yeast Sir 2. 

The Sirt1 gene in mice was disrupted by 

homologous recombination in 

embryonic stem cells. The majority of 

Sirt1 (¥/¥) embryos die between E9.5 

and E14.5, displaying altered histone 

modification, increased chromosomal 

aberrations, and impaired DNA damage 

repair. Tumor formation was increased 

in mutant tissues in Sirt1(+/¥): p53(+/ 

¥) double heterozygotes, indicating that 

full levels of Sirt1 are necessary for 

tumor suppression. Tumorigenesis is 

reduced by treatment with the 

polyphenol, resveratrol, which activates 

Sirt1. Sirt1 may act as a tumor 

suppressor by promoting DNA damage 

repair and maintaining genome 

integrity. Sirt1also is involved in the 

regulation of proteins involved in 

energy metabolism, and components of 

the circadian clock. 

Potential Commercial Applications: 

Oncology, Metabolism. 

Developer of Mouse: Chuxia Deng, 

Ph.D. (NIDDK). 

Relevant Publication: Wang RH, et al. 

Impaired DNA damage response, 

genome instability, and tumorigenesis 

in SIRT1 mutant mice. Cancer Cell. 

2008 Oct 7;14(4):312–23. [PMID 

18835033] 

Intellectual Property: HHS Reference 

No. E–120–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Jennifer S. Wong; 

301–435–4633; wongje@mail.nih.gov. 

Stat1LoxP (Stat1tm1Mam) Mouse Model 

for Oncology and Immunology Studies 

Description of Mouse: Selective 

inactivation of Stat1 in mammary cells 

indicates that its effect as a tumor 

suppressor in breast is direct. 

STAT1 is considered a tumor 

suppressor, but it is not known if this 

effect occurs directly in mammary cells 

or secondarily by disrupting interferon 

signaling through the JAK/STAT1 

pathway to induce immune responses. 

ERBB2/neu-induced breast cancer 

appeared sooner in mice lacking STAT1 

only in mammary cells than in wildtype mice, indicating that STAT1 tumor 

suppression was intrinsic to mammary 

cells and not secondary to an induced 

immune response. 

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24504 Federal Register / Vol. 77, No. 79 / Tuesday, April 24, 2012 / Notices 

Potential Commercial Applications: 

Oncology, Immunology. 

Developer of Mouse: Lothar 

Hennighausen, Ph.D. (NIDDK). 

Relevant Publication: Klover PJ, et al. 

Loss of STAT1 from mouse mammary 

epithelium results in an increased Neuinduced tumor burden. Neoplasia. 2010 

Nov;12(11):899–905. [PMID 21076615]. 

Intellectual Property: HHS Reference 

No. E–111–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Mojdeh Bahar, J.D., 

CLP; 301–435–2950; 

baharm@mail.nih.gov. 

Tg(Wap-cre)11738Mam Mouse Model 

for Developmental Biology Studies 

Description of Mouse: Crerecombinase under the control of the 

whey acidic acid protein was only 

detected in alveolar epithelial cells of 

mammary tissue during lactation, and 

transcription occurred at all stages of 

mammary development. 

The Cre recombinase from 

bacteriophage P1 excises intervening 

DNA sequences located between two 

unidirectional lox sites positioned on 

the same linear DNA segment, leaving 

one lox site behind. Through insertion 

of lox sites via homologous 

recombination into the gene of interest 

and targeting Cre recombinase 

expression to a specific cell type using 

a tissue-specific promoter, it is possible 

to introduce predetermined deletions 

into the mammalian genome. To delete 

genes specifically from mammary gland, 

transgenic mice were created carrying 

the Cre gene under the control of the 

whey acidic protein (WAP) gene 

promoter. Expression of WAP–Cre was 

only detected in alveolar epithelial cells 

of mammary tissue during lactation. 

Recombination mediated by Cre under 

control of the WAP gene promoter was 

largely restricted to the mammary gland 

but occasionally was observed in the 

brain. High-level transcriptional activity 

of WAP-based transgenes can be 

obtained at every stage of mammary 

development. 

Potential Commercial Application: 

Developmental Biology. 

Developer of Mouse: Lothar 

Hennighausen, Ph.D. (NIDDK). 

Relevant Publication: Wagner KU, et 

al. Cre-mediated gene deletion in the 

mammary gland. Nucleic Acids Res. 

1997 Nov 1;25(21):4323–30. [PMID 

9336464]. 

Intellectual Property: HHS Reference 

No. E–112–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Mojdeh Bahar, J.D., 

CLP; 301–435–2950; 

baharm@mail.nih.gov. 

Tg(MMTV–Cre)#Mam Mouse Model for 

Developmental Biology, Hepatology, 

and Oncology Studies 

Description of Mouse: Crerecombinase under the control of mouse 

mammary tumor virus long terminal 

repeat (MMTV) was expressed in the 

salivary gland and mammary epithelial 

cells of adult mice, and induced 

recombination in all tissues. 

The Cre recombinase from 

bacteriophage P1 excises intervening 

DNA sequences located between two 

unidirectional lox sites positioned on 

the same linear DNA segment, leaving 

one lox site behind. Through insertion 

of lox sites via homologous 

recombination into the gene of interest 

and targeting Cre recombinase 

expression to a specific cell type using 

a tissue-specific promoter, it is possible 

to introduce predetermined deletions 

into the mammalian genome. To delete 

genes specifically from mammary gland, 

transgenic mice were created carrying 

the Cre gene under the control of the 

mouse mammary tumor virus (MMTV) 

long terminal repeat (LTR). In adult 

MMTV–Cre mice, expression of the 

transgene was confined to striated 

ductal cells of the salivary gland and 

mammary epithelial cells in virgin and 

lactating mice. In contrast to WAP–Cre, 

however, Cre expression under control 

of the MMTV LR resulted in 

recombination in all tissues. 

Potential Commercial Applications: 

Developmental Biology, Hepatology, 

Oncology. 

Developer of Mouse: Lothar 

Hennighausen, Ph.D. (NIDDK). 

Relevant Publication: Wagner KU, et 

al. Cre-mediated gene deletion in the 

mammary gland. Nucleic Acids Res. 

1997 Nov 1;25(21):4323–30. [PMID 

9336464]. 

Intellectual Property: HHS Reference 

No. E–113–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Mojdeh Bahar, J.D., 

CLP; 301–435–2950; 

baharm@mail.nih.gov. 

Bcl-x LoxP (Bcl2l1tm1.1Mam) Mouse 

Model for Developmental Biology 

Studies 

Description of Mouse: Floxed Bcl-x: 

Conditional knockout of pro-survival 

Bcl-x in primordial germ cells was used 

to study the balance between proapoptotic Bax during embryogenesis. 

Bcl-x is a pro-survival protein that 

opposes the pro-apoptotic action of Bax 

which interacts with mitochondria to 

activate the caspase 9 pathway. Mice in 

which the Bcl-x gene is inactivated die 

at E12.5. To be able to study lineagespecific activities of Bcl-x at different 

stages of development, the Cre-LoxP 

recombination system was used. 

Homologous recombination was used to 

flank the promoter, exon1, and major 

coding exon2 of the Bcl-x gene with 

loxP sites. The targeted allele contained 

a loxP flanked (or floxed) neomycin 

cassette in the Bcl-x promoter, and an 

additional loxP site in intron 2. Floxed 

Bcl-x has been used to study the balance 

between Bcl-x and Bax in primordial 

germ cells that undergo controlled 

levels of cell reduction due to apoptosis, 

the induction of hemolytic anemia and 

splenomegaly following conditional 

deletion of the Bcl-x gene from 

erythroid cells, the protection of 

hepatocytes from apoptosis and ensuing 

fibrotic response by Bcl-x, and the 

demonstration that Bcl-x is critical for 

the survival of dendritic cells, important 

regulators of immune function. 

Potential Commercial Application: 

Developmental Biology. 

Developer of Mouse: Lothar 

Hennighausen, Ph.D. (NIDDK). 

Relevant Publication: Rucker EB 3rd, 

et al. Bcl-x and Bax regulate mouse 

primordial germ cell survival and 

apoptosis during embryogenesis. Mol 

Endocrinol. 2000 Jul;14(7):1038–52. 

[PMID 10894153]. 

Intellectual Property: HHS Reference 

No. E–115–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Mojdeh Bahar, J.D., 

CLP; 301–435–2950; 

baharm@mail.nih.gov. 

UTX LoxP Mouse Model for Oncology 

Research 

Description of Mouse: UTX-flox. 

Conditional knockout mice for the 

histone demethylase UTX (Kdm6a) 

conditional knockout will help 

understand its role as a tumor 

suppressor. 

Di- and tri-methylations on histone 

H3 lysine 27 (H3K27me2 and 

H3K27me3) are epigenetic marks for 

gene repression. UTX (ubiquitously 

transcribed X chromosome protein), also 

known as Kdm6a (lysine (K)-specific 

demethylase 6a) is a histone 

demethylase that specifically removes 

H3K27me2 and H3K27me3. UTX 

knockout mice are embryonic lethal, so 

we have generated UTX conditional 

knockout mice (UTX-flox) in which 

exon 24 is flanked with loxP sites. UTX 

has been found to be a tumor suppressor 

gene mutated in a wide variety of 

human cancers. The UTX-flox mice 

provide a valuable tool to study how 

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Federal Register / Vol. 77, No. 79 / Tuesday, April 24, 2012 / Notices 24505 

UTX functions as a tumor suppressor 

and as an epigenetic regulator of gene 

expression. 

Potential Commercial Application: 

Mouse model for Oncology research. 

Development Stage: Pre-clinical. 

Developer of Mouse: Kai Ge, Ph.D. 

(NIDDK). 

Relevant Publication: Unpublished. 

Gene ID: 22289. 

Intellectual Property: HHS Reference 

No. E–118–2012/0—Research Tool. 

Patent protection is not being pursued 

for this technology. 

Licensing Contact: Mojdeh Bahar, J.D., 

CLP; 301–435–2950; 

baharm@mail.nih.gov. 

Dated: April 18, 2012. 

Richard U. Rodriguez, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. 2012–9775 Filed 4–23–12; 8:45 am] 

BILLING CODE 4140–01–P 

ADVISORY COUNCIL ON HISTORIC 

PRESERVATION 

ACHP Quarterly Business Meeting 

AGENCY: Advisory Council on Historic 

Preservation. 

ACTION: Notice. 

SUMMARY: Notice is hereby given that 

the Advisory Council on Historic 

Preservation (ACHP) will meet 

Thursday, May 10, 2012. The meeting 

will be held in the Caucus Room of the 

Russell Senate Office Building at 

Constitution and Delaware Avenues 

NE., Washington, DC at 8:30 a.m. 

The ACHP was established by the 

National Historic Preservation Act of 

1966 (16 U.S.C. 470 et seq.) to advise the 

President and Congress on national 

historic preservation policy and to 

comment upon federal, federally 

assisted, and federally licensed 

undertakings having an effect upon 

properties listed in or eligible for 

inclusion in the National Register of 

Historic Places. The ACHP’s members 

are the Architect of the Capitol; the 

Secretaries of the Interior, Agriculture, 

Defense, Housing and Urban 

Development, Commerce, Education, 

Veterans Affairs, and Transportation; 

the Administrator of the General 

Services Administration; the Chairman 

of the National Trust for Historic 

Preservation; the President of the 

National Conference of State Historic 

Preservation Officers; a Governor; a 

Mayor; a Native American; and eight 

non-federal members appointed by the 

President. 

Call to Order—8:30 a.m. 

I. Chairman’s Welcome 

II. Chairman’s Award 

III. Chairman’s Report 

IV. ACHP Management Issues 

A. Credentials Committee Report and 

Recommendations 

B. Alumni Foundation Report 

C. Recodification of the National 

Historic Preservation Act 

V. Forum Discussion-Federal Budget 

Austerity and Historic PreservationPart II 

VI. Historic Preservation Policy and 

Programs 

A. Building a More Inclusive 

Preservation Program 

B. Legislative Agenda 

C. Rightsizing Task Force Report 

D. Sustainability Task Force Report 

VIII. Section 106 Issues 

A. Guidance on Coordinating and 

Substituting NEPA and Section 106 

Compliance 

B. Section 3 Report Submission and 

Follow up 

C. Traditional Cultural Landscapes 

Forum Action Plan Implementation 

D. Section 106 Training InitiativesWebinars 

E. Executive Order on Infrastructure 

Projects 

F. Post Office Closures and Disposal 

IX. New Business 

X. Adjourn 

Note: The meetings of the ACHP are open 

to the public. If you need special 

accommodations due to a disability, please 

contact the Advisory Council on Historic 

Preservation, 1100 Pennsylvania Avenue 

NW., Room 803, Washington, DC 202–606– 

8503, at least seven (7) days prior to the 

meeting. For further information: Additional 

information concerning the meeting is 

available from the Executive Director, 

Advisory Council on Historic Preservation, 

1100 Pennsylvania Avenue NW., #803, 

Washington, DC 20004. 

Dated: April 18, 2012. 

John M. Fowler, 

Executive Director. 

[FR Doc. 2012–9783 Filed 4–23–12; 8:45 am] 

BILLING CODE 4310–K6–P 

DEPARTMENT OF HOMELAND 

SECURITY 

Federal Emergency Management 

Agency 

[Docket ID FEMA–2012–0007] 

Hazard Mitigation Assistance for Wind 

Retrofit Projects for Existing 

Residential Buildings 

AGENCY: Federal Emergency 

Management Agency, DHS. 

ACTION: Notice of availability; request 

for comments. 

SUMMARY: The Federal Emergency 

Management Agency (FEMA) is 

accepting comments on Hazard 

Mitigation Assistance for Wind Retrofit 

Projects for Existing Residential 

Buildings. 

DATES: Comments must be received by 

June 25, 2012. 

ADDRESSES: You may submit comments, 

identified by Docket ID FEMA–2012– 

0007, by one of the following methods: 

Federal eRulemaking Portal: http:// 

www.regulations.gov. Search for docket 

ID FEMA–2012–0007 and follow the 

instructions for submitting comments. 

Please note that this proposed policy is 

not a rulemaking and the Federal 

Rulemaking Portal is being utilized only 

as a mechanism for receiving comments. 

Mail/Hand Delivery/Courier: Office of 

Chief Counsel, Federal Emergency 

Management Agency, 500 C Street SW., 

Room 835, Washington, DC 20472– 

3100. 

FOR FURTHER INFORMATION CONTACT: 

Cecelia Rosenberg, Federal Insurance 

and Mitigation Administration, Federal 

Emergency Management Agency, 1800 

South Bell Street, Room 608, Arlington, 

VA 20598–3015, (phone) 202–646–3321, 

or email 

cecelia.rosenberg@fema.dhs.gov. 

SUPPLEMENTARY INFORMATION: 

I. Public Participation 

Instructions: All submissions received 

must include the agency name and 

docket ID. Regardless of the method 

used for submitting comments or 

material, all submissions will be posted, 

without change, to the Federal 

eRulemaking Portal at http:// 

www.regulations.gov, and will include 

any personal information you provide. 

Therefore, submitting this information 

makes it public. You may wish to read 

the Privacy Act notice which can be 

viewed by clicking on the ‘‘Privacy 

Notice’’ link in the footer of 

www.regulations.gov. 

Docket: The proposed policy is 

available in docket ID FEMA–2012– 

0007. For access to the docket to read 

background documents or comments 

received, go to the Federal eRulemaking 

Portal at http://www.regulations.gov and 

search for the docket ID. Submitted 

comments may also be inspected at 

FEMA, Office of Chief Counsel, Room 

835, 500 C Street SW., Washington, DC 

20472. 

II. Background 

The Pre-Disaster Mitigation program 

(PDM) and the Hazard Mitigation Grant 

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