the present invention relates to the critical dosages and timing of administration of rhcc10 to treat , cure or prevent rds , bdp , chronic lung disease and / or pulmonary fibrosis , asthma , and copd in humans . rhcc10 is preferably obtained by the processes described in u . s . patent application publication nos . us 2003 - 0109429 and us 2003 - 0207795 , both of which are incorporated by reference in their entirety , or via any other process which yields pharmacutical grade rhcc10 . the rhcc10 of the embodiments of the present invention may also be administered by the intratraceal , endotracheal , dialysate , ophthalmic , intravenous , systemic , or oral routes . furthermore the rhcc10 of the embodiments of the present invention may be administered with , without , before or after surfactant therapy . preferably , in treating or preventing rds or bpd rhcc10 is administered during the first day of an infant patient &# 39 ; s life . more preferably , rhcc10 is administered as soon as medically possible during the first day of an infant patient &# 39 ; s life , for example , and without limitation , within about 30 minutes of intubation and receipt of surfactant . premature infants are typically intubated for the purposes of administering oxygen and inflating their lungs , which would collapse without intubation . intubation can then serve as a direct route for the intratracheal administration ( also known as endotracheal administration ) of medicines , such as surfactants , to the lungs . thus the preferred route of administration for rhcc10 is also intratracheal administration , however alternate routes of administration are also possible such as inhalation , inhalation of pegylated rhcc10 , injection into the muscle tissues , intravenous injection , intranasal administration , oral administration and administration by suppository . rhcc10 may also be administered to treat , cure or prevent chronic lung disease and / or pulmonary fibrosis , asthma , and copd . based on the results described herein , rhcc10 will have therapeutic benefit to patients suffering from chronic lung disease and / or pulmonary fibrosis , asthma , and copd . more specifically , and as shown below , rhcc10 , when dosed at the amounts described below , lowers neutrophil counts , il - 6 levels and il - 8 levels in humans , and thus will provide an effective treatment rds , asthma and copd . one method of measuring the therapeutic effect of rhcc10 on a patient is to measure conditions present in the tracheal aspirate fluid , which is indicative of conditions present in the tracheal and bronchoalveolar fluid of the patient &# 39 ; s lungs . such conditions may be one or more of the following : il - 6 levels , il - 8 levels , total neutrophil counts , total cell counts and total protein concentration . a method of measuring the concentration of cc10 in a patient , and thus determining whether treatment has established therapeutically effective levels of cc10 in the patient , may include one or more of following : measuring cc10 concentration in taf , serum or urine . with reference to the following embodiments , rhcc10 may be administered to achieve certain desired effects , establishing that therapeutically effective levels of cc10 have been achieved in the patient , while at the same time avoiding other deleterious effects . for example , rhcc10 may be administered to achieve concentrations of cc10 in the tracheal aspirate fluid which exceed the deficient production of endogenous cc10 by the premature infant . rhcc10 may also be administered to achieve early peak serum concentrations of rhcc10 in patients , for example within about 6 hours after administration . as a further example , when administered in accordance with the described methods , rhcc10 administration may also achieve a peak concentration in urine at about 12 hours for example . as yet another example , rhcc10 may be administered so as to achieve significantly lower cell counts , neutrophil cell counts , protein concentrations , il - 6 levels and il - 8 levels in the patient &# 39 ; s tracheal aspirate fluid and in the patient &# 39 ; s lungs . furthermore , rhcc10 may be administered such that it does not significantly reduce the patient &# 39 ; s endogenous cc10 production , inhibit platelet aggregation or cause an adverse immunologic reaction . to effectuate the desired outcomes which are further described below , reference is made to methods of administration described in the following embodiments : in one embodiment , a dose or multiple doses of rhcc10 equaling a dose ranging from about 1 . 5 to about 5 mg / kg of body mass may be administered . in another embodiment a dose or multiple doses of rhcc10 equaling a dose ranging from about 15 nanograms / kg of body mass to about 10 mg / kg of body mass is administered . in still another embodiment a dose or multiple doses of rhcc10 equaling a dose ranging from about 0 . 15 mg / kg and about 5 mg / kg of patient body mass is administered . in yet another embodiment the above doses of rhcc10 may be administered intratracheally to the patient . in yet another embodiment , the above doses of rhcc10 may be administered to the patient by aerosol . in a further embodiment rhcc10 , in accordance with the methods described above , may be administered prior to , during or after surfactant therapy . in still another embodiment , rhcc10 , in accordance with the methods described above , may be administered to treat rds , bpd , asthma , chronic lung disease , pulmonary fibrosis or copd in a patient . the doses of rhcc10 described above may be administered daily , more than once daily , every other day or in a tapered fashion depending upon the severity of disease being treated , the patient &# 39 ; s overall health , and whether an acute or chronic condition is being treated . for example , the more severe the disease condition , a higher the amount of rhcc10 would be required to effectively treat the disease . for maintenance therapy of chronic disease , for example , to prevent an exacerbation of chronic asthma , rds , copd , bdp or other pulmonary condition , lower doses would be required . it is understood that a physician would be able to monitor and adjust doses as needed based on the patient &# 39 ; s symptoms and responses to therapy and within the parameters and dose ranges described in the embodiments of the present invention . the following detailed examples are illustrations of embodiments . it should be clear that these are not intended to limit the scope of the present invention . patients were enrolled in a placebo - controlled , blinded , dose ranging study at four hospital sites . rhcc10 was produced in e . coli bacteria and purified by a proprietary process ( claragen , inc ., college park , md . ), described in u . s . application publication nos . us 2003 - 0109429 and us 2003 - 0207795 , both of which are incorporated by reference in their entirety . the protein for the study was provided as a & gt ; 98 % pure solution of recombinant human cc10 homodimer . the biological activity of each batch was compared using a proprietary secretory pla 2 inhibition assay , described in u . s . application publication nos . us 2002 - 0169108 which is incorporated herein by reference . newborn infants who met the following criteria were enrolled : 1 ) age ≦ 24 h ; 2 ) birth weight between 700 and 1 , 300 g ; 3 ) gestational age ≧ 24 wk ; 4 ) diagnosis of rds based on clinical and radiographic criteria ; 5 ) requirement for intubation and mechanical ventilation ; 6 ) receipt of surfactant , 100 mg / kg ( survanta , ross laboratory ). patients could be given subsequent doses of surfactant if clinically indicated following rhcc10 administration . table 1 depicts the composition of the study groups ( cohorts ): rhcc10 , was formulated in a volume of 2 ml / kg of sterile , unbuffered saline . patients were enrolled in two cohorts , each comparing study drug to placebo . the first cohort consisted of 12 patients , randomized so that one - third received placebo and the other two - thirds received rhcc10 at 1 . 5 mg / kg of body mass of the study drug . after the first cohort of patients was enrolled and the safety data reviewed by the dsmc , a second cohort of 12 patients was enrolled . they were also randomized so that one - third received placebo and the other two - thirds received rhcc10 at 5 . 0 mg / kg of body mass . each patient then received a single dose of the study drug ( or placebo ) as soon as possible after surfactant replacement therapy , but not longer than 4 h after surfactant . study drug or placebo was administered intratracheally ( it ) in two equal aliquots via a pre - measured feeding tube placed into the distal third of the endotracheal tube , with the patient in the right and then left lateral decubitus position and 30 ° of trendelenburg . as described in greater detail in examples 2 - 4 , pharmacokinetic analyses were conducted on samples of taf , serum , and urine samples and analyses of cells counts and protein levels were performed on samples of taf . taf was obtained by instilling 1 ml of saline into the endotracheal tube and suctioning the fluid into a leuken &# 39 ; s trap . the catheter was then washed with an additional 1 ml saline . in some cases the first tracheal aspirate was obtained prior to surfactant administration ( baseline ). subsequent taf collections were obtained at 12 , 24 , 48 and 72 hours post - administration . taf was only collected if infants continued to require intubation and mechanical ventilation . the taf was centrifuged at 300 × g for 10 minutes to pellet the cells . the supernatant was removed and frozen at − 70 ° c . the pharmacokinetic analysis was conducted on samples of taf , serum , and urine samples using a competitive elisa for human cc10 developed by the sponsor . the assay utilizes a single anti - human cc10 polyclonal antibody as a capture reagent . cc10 in the sample competes with a synthetic cc10 - hrp ( horseradish peroxidase ) conjugate for antibody binding sites in the plate wells . thus , the signal decreases with increasing cc10 concentration in the sample . samples were run in duplicate and a standard curve was run for each set of assays using rhcc10 calibrators . the limit of detection is 5 ng / ml and the results were reproducible with coefficients of variation typically under 20 %. the assay does not appear to distinguish between native and recombinant cc10 , thus total cc10 levels were measured . immunogenicity of the study drug was assessed by titration of anti - c10 antibodies in serum obtained at 28 days post administration . referring to examples 5 - 8 below , analyses for pulmonary inflammatory markers were performed as follows : the taf cell pellet was resuspended and cell counts performed using a hemocytometer . differential cell counts in taf were determined by cytocentrifugation and differential staining . total protein in taf was measured using the pierce bca technique , and a panel of cytokines ( multiplex cytokine analysis , luminetics corp .) was measured in taf from all three experimental groups at 0 , 24 and 48 hours post - administration . il - 6 and il - 8 cytokines were measured in taf from patients in all three groups at times 0 , 1 and 2 days ( with a minimum of three and maximum of seven samples / group ). concentrations of cc10 and analysis of inflammatory markers over time were examined by using mixed model analysis of variance to test the interaction of time and dose . non - parametric testing was performed when unequal variance was detected . sample characteristics , the incidence of complications and clinical outcomes were analyzed by fisher &# 39 ; s exact test for categorical variables or one way analysis of variance for continuous variables . with reference to fig1 it has been found that during the first 48 hours of life , after an initial dose of rhcc10 , significantly increased overall cc10 concentration occurred in patients receiving rhcc10 in dosages comprising either 1 . 5 mg / kg of body mass or 5 mg / kg of body mass versus placebo . thus , administration of rhcc10 during the first 24 hours of life has a significant positive impact on cc10 levels in patients during the first two days of life . furthermore , administration of rhcc10 will increase overall cc10 concentrations in patients . reference is now made to table 2 , as well as to fig1 , the contents of which are further described in this example . cc10 concentrations in patients were measured at 12 , 24 , 48 and 72 hours post - administration . an average concentration for each patient group receiving a particular dose of rhcc10 ( 1 . 5 or 5 mg / kg ) or placebo was determined as follows . cc10 concentrations in taf were observed for time points where there were at least three patient samples per group ( fig1 ). this allowed for analysis of taf samples for all groups following administration of placebo ( 0 . 9 % sterile saline ) or rhcc10 through day 3 of life . for safety and logistical reasons , samples were not obtained if surfactant had recently been administered or if the infant had been extubated . at 12 hours of life , cc10 concentrations in taf from infants treated with the study drug was significantly higher than the placebo group , but there was little difference between the two groups who received rhcc10 . over the first 3 days of life , cc10 concentrations in taf from infants receiving placebo generally increased , whereas cc10 levels in treated infants tended to remain constant ( 1 . 5 mg / kg of body mass ) or decrease ( 5 mg / kg of body mass ). however , cc10 levels from infants receiving placebo did not exceed the cc10 levels of those infants receiving rhcc10 in either 1 . 5 mg / kg of body mass or 5 mg / kg of body mass dosages during the first 48 hours of life . those infants receiving 1 . 5 mg / kg of body mass rhcc10 had the highest levels of cc10 at 48 hours . furthermore , with reference to fig2 , in one embodiment , rhcc10 may be administered intratracheally such that peak serum levels of cc10 are achieved within 6 hours of administration . peak serum levels occur within 6 hours , irrespective of the dose of rhcc10 administered . based on the results described below and in fig2 , peak serum levels will occur within about 6 hours after administration across all dosage ranges . reference is now made to table 3 , as well as to fig2 , the contents of which are further described in this example . in determining average peak serum levels , blood ( 0 . 3 ml ) was obtained for the measurement of serum concentration of cc10 before drug administration ( 0 hours ) and at 6 , 12 , 24 , 36 , and 48 hours after administration of rhcc10 . an average concentration for each patient group receiving a particular dose of rhcc10 or placebo was determined . serum concentrations of cc10 were similar in all 3 groups before treatment ( fig2 ). infants who received rhcc10 had substantially higher serum concentrations than infants receiving placebo and this varied in a dose dependent manner . average peak serum levels after administration of rhcc10 may range from about 1290 ng / ml of serum to about 2800 ng / ml serum when rhcc10 is given in a single dose of between 1 . 5 mg / kg of body mass and 5 mg / kg of body mass . as shown in table 3 , the elimination half - life of a rhcc10 dosage of 1 . 5 mg / kg of body mass was about 11 . 6 hours , whereas the elimination half - life of a rhcc10 dose of 5 mg / kg of body mass was about 9 . 9 hours . cc10 concentrations in the serum of treated infants were comparable to placebo levels within 48 hours of administration . referring to fig3 , in one embodiment , rhcc10 may also be administered intratracheally at the above - mentioned dosages such that peak cc10 levels in urine occur 12 hours after administration . for example , cc10 concentrations in the urine of treated infants increase in a largely dose - dependent manner , but are comparable to placebo levels within 48 h of administration . reference is now made to table 4 , as well as to fig3 , the contents of which are further described in this example . urine samples were obtained at 12 , 24 , 36 and 48 hours after administration of rhcc10 . each urine sample consisted of the total volume voided over the previous 12 hours . in urine , cc10 concentrations in treated infants increased in a largely dose - dependent manner , but were comparable to placebo levels within 48 h of administration ( fig3 ). as shown in fig4 and in table 5 , total cell counts were performed on taf fluids and are shown in fig5 . average total cell counts were obtained by measuring and averaging total cell counts in taf within the placebo and 5 mg / kg rhcc10 study groups . study groups were sampled at 0 . 5 , 1 , 2 , and 3 days post - administration . total cell counts were significantly lower in the 5 mg / kg group on days 1 - 3 compared to the placebo group . total cells counts were at least twice as low during days 1 - 3 of life after rhcc10 at 5 mg / kg of body mass was administered versus placebo . total neutrophil counts were performed on taf fluids in order to gauge rhcc10 &# 39 ; s effect on inflammation in the lungs and are shown in fig5 . inflammation of the lungs is caused by an excess of neutrophil cells which are a cause of rds , bdp , chronic lung disease , pulmonary fibrosis , asthma , and copd . average neutrophil counts were obtained by measuring and averaging neutrophil counts in taf within each study group ( placebo and 5 mg / kg rhcc10 ). study groups were sampled at 0 . 5 , 1 , 2 , and 3 days post - administration . neutrophil counts were significantly lower in the 5 mg / kg group relative to the placebo group . for example , on day two the placebo group &# 39 ; s neutrophil levels were over 30 cells × 10 ( 4 )/ ml of taf versus about 10 cells × 10 ( 4 )/ ml of taf for the group receiving rhcc10 at 5 mg / kg of body mass . therefore , excessive neutrophil cell amounts were minimized in the lungs . referring now to fig6 and to table 7 , total protein levels were measured in the taf of both treatment groups ( rhcc10 at 1 . 5 mg / kg and 5 mg / kg of body mass ) in order to gauge rhcc10 &# 39 ; s effect on protein leak and pulmonary edema . both protein leak and pulmonary edema are conditions damaging to the lungs and symptomatic of rds , bdp , chronic lung disease , pulmonary fibrosis , asthma , and copd . average total protein concentrations were obtained by measuring and averaging total protein concentrations in taf within each study group ( placebo , 1 . 5 mg / kg rhcc10 and 5 mg / kg rhcc10 ). study groups were sampled at 0 . 5 , 1 , 2 , and 3 days post - administration . total protein was significantly lower in taf from both treatment groups compared to placebo . for example , by day three post - administration , total protein in the taf of the placebo group was nearly 1000 μg / ml of taf whereas total protein in the treatment groups on day three did not exceed 350 μg / ml of taf . thus protein leak and pulmonary edema had been minimized in the treatment groups . il - 6 cytokine was measured in taf from patients in all three groups at times 0 , 1 and 2 days post - administration ( with a minimum of three and maximum of seven samples / group ). referring now to table 8 and fig7 , il - 6 concentrations were effectively reduced by the study drug ( rhcc10 in saline ) in both groups , but increased over time in the placebo group . for example , those patients receiving rhcc10 at 5 mg / kg of body mass had il - 6 levels below 200 pg / ml of taf over the first two days following administration . those patients receiving rhcc10 at 1 . 5 mg / kg of body mass had il - 6 levels below 300 pg / ml of taf over the first two days post - administration and had an il - 6 level below 100 pg / ml by day two . however , those patients on placebo had steadily increasing il - 6 levels , exceeding 400 pg / ml by day 2 . thus rhcc10 , when administered according to the present teachings , reverses the upward trend of il - 6 levels in patient lungs , thus preventing neutrophil influx to the lung . total il - 8 levels in taf and serum in patients treated with rhcc10 referring now to fig8 and table 9 , il - 8 cytokine was measured in taf from patients in all three groups at 48 hours post - administration . il - 8 is a potent chemoattractant for neutrophils and other circulating inflammatory cells , that is released by local epithelial cells , resident immune cells , and fibroblasts in response to injury or irritation . il - 8 levels were lower in rhcc10 - treated patients than in patients receiving placebo . administration of rhcc10 , as depicted above , reduced the levels of il - 8 released from the lungs and into the systemic circulation . thus , this data shows that rhcc10 is effective at treating or preventing rds , bdp , chronic lung disease and / or pulmonary fibrosis , asthma , and copd by lowering il - 8 levels and thus treating the causative agent of these diseases . table 10 depicts comparative outcomes of patients who received rhcc10 versus patients who received placebo . patients were monitored at six months of corrected age ( the developmental timepoint at which they would have been six months old had they been born at the normal 40 weeks of gestation .) table 11 depicts further comparative outcomes of patients who received rhcc10 versus patients who received placebo . referring to table 10 above , patients who received rhcc10 therapy had reduced incidences of respiratory symptoms , e . g . coughing and wheezing . coughing and wheezing are symptoms common rds , bdp , chronic lung disease and / or pulmonary fibrosis , asthma , and copd . after receiving rhcc10 , patients had fewer doctor visits due to respiratory symptoms , and no patients were hospitalized for breathing problems in comparison to 50 % of infants in the placebo group who were hospitalized for their respiratory symptoms . this data shows that rhcc10 significantly reduces the severity of respiratory symptoms , preventing the need for rehospitalization . referring to table 11 above , the therapeutic effect of rhcc10 on short term respiratory distress is reflected in the decreased requirement for additional doses of exogenous surfactant therapy . the length of hospital stays was tabulated for each study group . only 28 . 6 % of patients in the low dose group were still hospitalized after 36 weeks compared to 71 . 4 % of patients in the placebo group and 66 . 7 % in the high dose groups . patients in the low dose rhcc10 group ( 1 . 5 mg / kg of body mass ) were on the ventilator and ncpap for significantly fewer days than the placebo patients . when total days of mechanical ventilation were evaluated , there was also a trend towards a reduction in the need for ventilatory support in the low dose group ( the 1 . 5 mg / kg body mass group ). these results show that rhcc10 therapy , when administered in accordance with the present teachings , decreased the severity of rds compared to placebo and reduced or eliminated the incidence of respiratory problems severe enough to warrant medical attention or rehospitalization . furthermore , this data shows that the safety profile of rhcc10 is superior to other anti - inflammatory agents such as corticosteroids . the safety and tolerability of the study drug were assessed through 36 weeks pca ( post conceptual age , also known as pma — post menstrual age ) by comparing the incidence of adverse events in the treatment and placebo groups and to the historical incidence of the adverse events at each institution . no deaths were attributable to administration of rhcc10 . in addition , a preliminary assessment of the efficacy of it rhcc10 in decreasing the incidence of bpd was made on the basis of the following data : duration of mechanical ventilation , oxygen requirement at 28 days with an abnormal chest radiograph , oxygen requirement at 36 weeks pca or date of discharge . growth parameters were assessed at birth , 28 days of age and 36 weeks pca , blood chemistries and liver function tests were evaluated at the onset of the study and on days 7 and 28 post - administration . complete blood counts and urinalysis were performed on enrollment , 24 , 48 and 72 h , 7 and 28 d post - administration . cranial ultrasounds were performed upon randomization and were repeated at 7 and 28 d of life . there were no instances of pvl ( peri - ventricular leukomalacia ) in the rhcc10 - treated infants . however , there was one infant in the placebo group who developed pvl . pvl occurs when leukocytes ( primarily neutrophils ) infiltrate the brain and cause a severe inflammatory response . pvl , if not lethal , typically results in severe neurological impairment in the infant . smaller and younger infants are predisposed to pvl . even though the infants in the high dose group ( 5 . 0 mg / kg patient body mass ) were smaller and younger than in the placebo group , there was no pvl in the high dose group . rhcc10 thus protected these disadvantaged infants from pvl . likewise , the incidence of ivh ( intraventricular hemorrhage ), which occurs when a blood vessel in the brain bursts in response to aggressive ventilation and high oxygen levels , was lower in the rhcc10 treated groups than in the placebo group . rhcc10 appears to have protected these disadvantaged infants in the high dose group from ivh , refuting the scientific papers that taught that rhcc10 inhibits platelet aggregation and would promote hemorrhaging in vivo . pda ( patent ductus arteriosis ), a defect or incomplete closure in the walls of the heart , was significantly decreased in the rhcc10 - treated groups compared to placebo . pda is a life - threatening problem that must be corrected surgically , if it is not resolved in the first several months of life . rhcc10 reduced the incidence of pda , possibly by decreasing the stress on the heart . there were no significant differences in values obtained for blood chemistries , complete blood counts or results of urinalysis among groups at any of the time points evaluated . there were no significant differences in the incidence of non - respiratory adverse events in the treatment and placebo groups ( table 2 ). three cases of nec occurred at one center in rhcc10 - treated infants . however , other premature infants not enrolled in the study at that center also developed nec at the same time . growth parameters were similar among the groups . it will be further appreciated that the safety of rhcc10 can be measured by conducting an analysis of the potential immunogenicity of the administered rhcc10 using plasma samples . plasma samples collected on day 28 of life were tested for the presence of anti - cc10 antibodies . no evidence of antibody formation was present in any of the 28 day plasma samples from any of the groups . with reference to table 2 , there were no significant differences in the incidence of non - respiratory adverse events in the treatment and placebo groups . three cases of nec occurred at one center in rhcc0 - treated infants . however , other premature infants not enrolled in the study at that center also developed nec at the same time . growth parameters at 36 weeks cga were similar among the groups . similarly , there were no significant differences in values obtained for blood chemistries , complete blood counts or results of urinalysis among groups at any of the time points evaluated . thus , rhcc10 administration , in contrast to corticosteroids , did not appear to cause any significant safety issues in premature infants . in addition , it rhcc10 did not elicit an immunogenic response from treated infants . the only adverse event that was increased in treated infants compared to placebo controls was nec ( p = ns ), however , it was not possible to attribute the nec to the administration of rhcc10 for two reasons . first , excess cc10 was cleared from all infants by 48 h post - administration and the 3 cases of confirmed nec occurred 3 - 6 wk post - administration . second , all cases of confirmed nec occurred at the same center . in addition , there were other cases of nec in infants not enrolled in the rhcc10 study in this center occurring in the same timeframe , suggesting an outbreak pattern . these data indicate it is highly unlikely that rhcc10 administration was related to the development of nec . referring now to , for example , examples 10 - 13 , it has been shown that rhcc10 is safe and well - tolerated because , upon administration to a patient , it does not elicit any immediate or delayed local or systemic reactions in the patient , it is not associated with any unusual adverse events , or increased severity or frequency of typical adverse events for the treated patient population , as described above . furthermore , rhcc10 is safe and well - tolerated because it does not elicit any immunologic response from the patient to either the rhcc10 or to endogenous cc10 does not predispose the patient to bleeding or hemorrhage , or specifically increase the platelet aggregation time in the patient , and does not compromise the patient &# 39 ; s immune function and predispose the patient to infection . a patient , who may be an adult , child or a premature infant presents with rds , bdp , chronic lung disease ( in the case of a child or an adult ), pulmonary fibrosis ( in the case of a child or an adult ), asthma , or copd . a dose of rhcc10 from 1 . 5 mg / kg to 5 mg / kg of patient body mass is given to the patient . the patient will then demonstrate a resolution of the symptoms of the aforementioned condition . a patient , who may be an adult , child or a premature infant presents with rds , bdp , chronic lung disease ( in the case of a child or an adult ), pulmonary fibrosis ( in the case of a child or an adult ), asthma , or copd . a dose of rhcc10 from 0 . 15 ng / kg to 5 mg / kg of patient body mass is given to the patient . the patient will then be relieved of the symptoms of the aforementioned condition . a patient , who may be an adult , child or a premature infant presents with rds , bdp , chronic lung disease ( in the case of a child or an adult ), pulmonary fibrosis ( in the case of a child or an adult ), asthma , or copd . a dose of rhcc10 from 0 . 15 mg / kg to 5 mg / kg of patient body mass is given to the patient . the patient will then be relieved of the symptoms of the aforementioned condition . based on the foregoing , the critical ranges for rhcc10 dosages effective to safely treat , cure and prevent rds , bdp , chronic lung disease and / or pulmonary fibrosis , asthma , and copd have been found . accordingly , the present invention provides a safe and well - tolerated rhcc10 based therapy effective at treating the symptoms of rds , bdp , chronic lung disease and / or pulmonary fibrosis , asthma , and copd thus increasing the long term survivability of both premature infants , child and adult patients suffering from these conditions , while not causing any dangerous side effects .
the present invention relates generally to the use of recombinant human cc10 , also known as recombinant human uteroglobin , for use as a therapeutic in the treatment of respiratory distress syndrome , bronchopulmonary dysplasia , chronic lung disease and / or pulmonary fibrosis , asthma and chronic obstructive pulmonary disease . more particularly , the invention provides methods , including broadly the critical dosage ranges of rhcc10 , which may be administered to safely and effectively treat the aforementioned conditions . the invention further provides a composition useful in administering rhcc10 to humans .