NON-INVASIVE SYSTEMS AND METHODS FOR IN-SITU PHOTOBIOMODULATION

• US 20100016783A1
• Filed: 04/03/2009
• Published: 01/21/2010
• Est. Priority Date: 04/04/2008
• Status: Abandoned Application

• Current Assignee: Duke University, Immunolight, LLC
• Original Assignee: Duke University, Immunolight, LLC
• Inventors: Vo-Dinh, Tuan, Walder, Harold, BOURKE, Frederic J. JR.
• Application Number:
  US12/417,779
• Publication Number:
  US 20100016783A1
• Time in Patent Office: Days
• US Class Current: 604/20
• CPC Class Codes: A61K 41/0057 Photodynamic therapy with a photosensitizer, i.e. agent able to produce reactive oxygen species upon exposure to light or radiation, e.g. UV or visible light; photocleavage of nucleic acids with an agent
• CPC Class Codes: A61K 41/0061 5-aminolevulinic acid-based PDT: 5-ALA-PDT involving porphyrins or precursors of protoporphyrins generated in vivo from 5-ALA
• CPC Class Codes: A61K 47/6923 the form being an inorganic particle, e.g. ceramic particles, silica particles, ferrite or synsorb
• CPC Class Codes: A61N 2005/0642 Irradiating part of the body at a certain distance
• CPC Class Codes: A61N 2005/0659 infrared
• CPC Class Codes: A61N 2005/0661 ultraviolet
• CPC Class Codes: A61N 2005/0662 Visible light
• CPC Class Codes: A61N 2005/1098 Enhancing the effect of the particle by an injected agent or implanted device
• CPC Class Codes: A61N 5/022 Apparatus adapted for a specific treatment
• CPC Class Codes: A61N 5/0618 Psychological treatment
• CPC Class Codes: A61N 5/062 Photodynamic therapy, i.e. excitation of an agent
• CPC Class Codes: A61N 5/0622 Optical stimulation for exciting neural tissue
• CPC Class Codes: A61N 5/10 X-ray therapy; Gamma-ray therapy; Particle-irradiation therapy A61N5/01 takes precedence
• CPC Class Codes: A61P 1/04 for ulcers, gastritis or reflux esophagitis, e.g. antacids, inhibitors of acid secretion, mucosal protectants
• CPC Class Codes: A61P 13/08 of the prostate
• CPC Class Codes: A61P 13/12 of the kidneys
• CPC Class Codes: A61P 17/02 for treating wounds, ulcers, burns, scars, keloids, or the like
• CPC Class Codes: A61P 19/02 for joint disorders, e.g. arthritis, arthrosis
• CPC Class Codes: A61P 19/08 for bone diseases, e.g. rachitism, Paget's disease
• CPC Class Codes: A61P 25/00 Drugs for disorders of the nervous system
• CPC Class Codes: A61P 25/02 : for peripheral neuropathies
• CPC Class Codes: A61P 25/04 : Centrally acting analgesics, e.g. opioids
• CPC Class Codes: A61P 25/08 : Antiepileptics; Anticonvulsants
• CPC Class Codes: A61P 25/16 : Anti-Parkinson drugs
• CPC Class Codes: A61P 25/28 : for treating neurodegenerative disorders of the central nervous system, e.g. nootropic agents, cognition enhancers, drugs for treating Alzheimer's disease or other forms of dementia
• CPC Class Codes: A61P 27/02 : Ophthalmic agents
• CPC Class Codes: A61P 29/00 : Non-central analgesic, antipyretic or antiinflammatory agents, e.g. antirheumatic agents; Non-steroidal antiinflammatory drugs [NSAID]
• CPC Class Codes: A61P 3/04 : Anorexiants; Antiobesity agents
• CPC Class Codes: A61P 31/00 : Antiinfectives, i.e. antibiotics, antiseptics, chemotherapeutics
• CPC Class Codes: A61P 31/04 : Antibacterial agents
• CPC Class Codes: A61P 31/12 : Antivirals
• CPC Class Codes: A61P 35/00 : Antineoplastic agents
• CPC Class Codes: A61P 35/02 : specific for leukemia
• CPC Class Codes: A61P 37/00 : Drugs for immunological or allergic disorders
• CPC Class Codes: A61P 37/04 : Immunostimulants
• CPC Class Codes: A61P 37/06 : Immunosuppressants, e.g. drugs for graft rejection
• CPC Class Codes: A61P 43/00 : Drugs for specific purposes, not provided for in groups A61P1/00-A61P41/00
• CPC Class Codes: A61P 9/10 : for treating ischaemic or atherosclerotic diseases, e.g. antianginal drugs, coronary vasodilators, drugs for myocardial infarction, retinopathy, cerebrovascula insufficiency, renal arteriosclerosis

Abstract

Products, compositions, systems, and methods for modifying a target structure which mediates or is associated with a biological activity, including treatment of conditions, disorders, or diseases mediated by or associated with a target structure, such as a virus, cell, subcellular structure or extracellular structure. The methods may be performed in situ in a non-invasive manner by application of an initiation energy to a subject thus producing an effect on or change to the target structure directly or via a modulation agent. The methods may further be performed by application of an initiation energy to a subject in situ to activate a pharmaceutical agent directly or via an energy modulation agent, optionally in the presence of one or more plasmonics active agents, thus producing an effect on or change to the target structure. Kits containing products or compositions formulated or configured and systems for use in practicing these methods.

Claims

1. A method for modifying a target structure which mediates or is associated with a biological activity comprising:

applying an initiation energy from at least one source to a target structure in a subject in need of treatment, wherein the initiation energy contacts the target structure and induces a predetermined change in said target structure in situ,

wherein said predetermined change modifies the target structure and modulates the biological activity of the target structure.

2. The method of claim 1, wherein said initiation energy is capable of penetrating completely through said subject.

3. The method of claim 1, wherein said initiation energy is applied from a single source.

4. The method of claim 1, wherein said initiation energy is applied from more than one source.

5. The method of claim 1, wherein said initiation energy generates light that induces a predetermined change in the target structure with or without an energy modulator or photoactive agent.

6. The method of claim 1, wherein said initiation energy produces plasmonics and/or exciton coupling enhanced light generation that induces a predetermined change in the target structure with or without an energy modulator and/or photoactive agent.

7. The method of claim 1, further comprising administering to said subject at least one energy modulation agent which adsorbs, intensifies or modifies said initiation energy into an energy that effects the predetermined change in said target structure.

8. The method of claim 7, wherein said energy modulation agent is specifically located around, on, or in said target structure.

9. The method of claim 7, wherein said energy modulation agent transforms the initiation electromagnetic energy into a photonic or another electromagnetic energy that effects the predetermined change in said target structure.

10. The method of claim 9, wherein said energy modulation agent decreases the wavelength of the initiation energy.

11. The method of claim 9, wherein said energy modulation agent increases the wavelength of the initiation energy.

12. The method of claim 1, in which said predetermined change results in destruction, lysis or inactivation of the target structure.

13. The method of claim 1, in which said predetermined change does not result in destruction or inactivation of the target structure.

14. The method of claim 1, in which said predetermined change enhances an activity of the target structure.

15. The method of claim 14, wherein the activity enhanced is energy emission from the target, which then mediates, initiates or enhances a biological activity of other target structures in the subject, or of a second target structure.

16. The method of claim 1, wherein the target structure is a eukaryotic cell.

17. The method of claim 1, wherein the target structure is a prokaryotic cell.

18. The method of claim 1, wherein the target structure is a subcellular structure.

19. The method of claim 18, wherein the subcellular structure is a cell membrane, a nuclear membrane, cell nucleus, nucleic acid, mitochondria, ribosome, or other cellular organelle or component.

20. The method of claim 1, wherein the target structure is an extracellular structure.

21. The method of claim 1, wherein the target structure is a virus or prion.

22. The method of claim 1, wherein the target structure is a cellular tissue.

23. The method of claim 1, wherein the predetermined change results in treatment of a condition, disorder or disease in said subject.

24. The method of claim 23, wherein said condition, disorder or disease is cancer.

25. The method of claim 23, wherein said condition, disorder or disease occurs in a soft tissue and/or cartilage.

26. The method of claim 23, wherein said condition, disorder or disease occurs in bone tissue.

27. The method of claim 23, wherein said condition, disorder or disease is chronic pain.

28. The method of claim 23, wherein said condition, disorder or disease is at least one autoimmune disease.

29. The method of claim 1, wherein said predetermined change comprises wound healing.

30. The method of claim 1, wherein said predetermined change comprises enhancement of tissue growth, nerve regeneration or sensory regeneration/restoration.

31. The method of claim 23, wherein said condition, disorder or disease is a prion, viral, bacterial, fungal, or parasitic infection.

32. The method of claim 1, wherein said predetermined change comprises reduction or removal of fat deposits (liposuction).

33. The method of claim 23, wherein said condition, disorder, or disease is characterized by varicose veins.

34. The method of claim 23, wherein said condition, disorder, or disease is characterized by an enlarged prostate.

35. The method of claim 23, wherein said condition, disorder, or disease is characterized by retinal injuries and other ocular diseases.

36. The method of claim 23, wherein said condition, disorder, or disease is Parkinson'"'"'s disease.

37. The method of claim 23, wherein said condition, disorder, or disease is characterized by a behavioral, perceptional and/or cognitive disorder.

38. The method of claim 1, wherein said predetermined change comprises nerve (brain) imaging and stimulation or direct control of brain cell activity with light.

39. The method of claim 1, wherein said predetermined change comprises modulation of cell death (apoptosis).

40. The method of claim 1, wherein said predetermined change comprises modulating cell growth and division.

41. The method of claim 1, wherein said predetermined change comprises modulation of an activity, quantity, or number of intracellular components in a cell.

42. The method of claim 1, wherein said predetermined change comprises modulation of an activity, quantity, or number of extracellular components produced by, excreted by, or associated with a cell.

43. The method of claim 1, wherein the initiation energy is UV radiation, visible light, IR radiation, x-rays, gamma rays, an electron beam, microwaves or radio waves.

44. The method of claim 7, wherein the initiation energy is UV-A, visible photon energy, or near infrared energy, x-rays, gamma rays, an electron beam, microwaves or radio waves.

45. The method of claim 1, wherein the initiation energy is generated in-situ in the subject.

46. The method of claim 1, further comprising applying a heat producing energy source to the target structure to generate heat in the target structure and enhance the induction of the predetermined change.

47. The method of claim 46, wherein the heat producing energy source and the initiation energy source are the same.

48. The method of claim 46, wherein the heat producing energy source and the initiation energy source are different from one another.

49. The method of claim 1, wherein the initiation energy is intensified by a nanoparticle or nanocluster of atoms before reaching the target structure in the subject.

50. The method of claim 7, wherein the initiation energy is intensified by a nanoparticle or nanocluster of atoms and is further absorbed by the energy modulation agent.

51. The method of claim 1, wherein a plasmonics-active agent is further applied which enhances or modifies the applied initiation energy, such that the enhanced initiation energy causes the predetermined change in said target structure by the plasmonics-active agent with or without an energy modulation agent.

52. The method of claim 7, wherein a plasmonics-active agent is further applied which enhances or modifies the applied initiation energy, such that the enhanced initiation energy is absorbed, intensified or modified by the energy modulation agent into the energy that effects the predetermined change in said target structure.

53. The method of claim 7, wherein the at least one energy modulation agent is one or more members selected from a biocompatible fluorescing metal nanoparticle, fluorescing metal oxide nanoparticle, fluorescing metal coated metal oxide nanoparticle, fluorescing dye molecule, gold nanoparticle, silver nanoparticle, gold-coated silver nanoparticle, a water soluble quantum dot encapsulated by polyamidoamine dendrimers, a luciferase, a biocompatible phosphorescent molecule, a combined electromagnetic energy harvester molecule, and a lanthanide chelate exhibiting intense luminescence.

54. The method of claim 51, wherein the plasmonics-active agent is a PEPST probe with multi plasmonics resonance mode.

55. The method of claim 51, wherein the plasmonics-active agent is a PEPST probe comprising plasmonics-active metal nanostructures.

56. The method of claim 55, wherein the metal nanostructures are nanospheres, nanorods, nanocubes, nanopyramid, nanoshells, multi-layer nanoshells and combinations thereof.

57. The method of claim 51, wherein the plasmonics-active agent is a PEPST probe with multiple structures for different plasmonics activation regimes.

58. The method of claim 57, wherein the plasmonics activation regime is NIR and/or X rays.

59. The method of claim 51, wherein the plasmonics-active agent is an exciton-induced phototherapy (EIP) probe possessing exciton properties.

60. The method of claim 1, wherein said predetermined change modifies the target structure and modulates the biological activity of the target structure thus treating a condition, disorder or disease affecting the target structure.

61. The method of claim 7, wherein the at least one energy modulation agent is activated prior to administration and after administration to the subject, the activated energy modulation agent is triggered to emit an energy that induces the predetermined change.

62. The method of claim 61, wherein the at least one energy modulation agent is an infrared-triggered phosphor.

63. A method for modifying a target structure which mediates or is associated with a biological activity, comprising:

(1) contacting said target structure with at least one activatable pharmaceutical agent (PA) that is capable of effecting a predetermined change in a target structure when activated, optionally in the presence of at least one member selected from the group consisting of energy modulation agents, plasmonics-active agents and combinations thereof; and

(2) applying an initiation energy from an initiation energy source to said target structure,

wherein the energy modulation agent, if present, upgrades or downgrades the initiation energy to an activation energy capable of activating the at least one activatable pharmaceutical agent;

wherein the plasmonics-active agent, if present, enhances or modifies the applied initiation energy or the activation energy generated by the energy modulation agent, or both; and

thus causing the predetermined change to the target structure to occur, wherein said predetermined change modifies the target structure and modulates the biological activity of the target structure.

64. The method of claim 63, wherein the administering step comprises administering (a) at least one activatable pharmaceutical agent and (b) at least one energy modulation agent.

65. The method of claim 64, wherein components (a) and (b) are coupled one to another.

66. The method of claim 63, wherein the administering step comprises administering (a) at least one activatable pharmaceutical agent and (c) at least one plasmonics-active agent.

67. The method of claim 66, wherein components (a) and (c) are coupled one to another.

68. The method of claim 63, wherein the administering step comprises administering (a) at least one activatable pharmaceutical agent, (b) at least one energy modulation agent and (c) at least one plasmonics active agent, wherein the at least one plasmonics active agent comprises at least one metal nanoparticle.

69. The method of claim 68, wherein at least two of components (a)-(c) are coupled one to another.

70. The method of claim 68, wherein all of components (a)-(c) are coupled one to another.

71. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe with multi plasmonics resonance mode.

72. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe comprising plasmonics-active metal nanostructures.

73. The method of claim 72, wherein the metal nanostructures are nanospheres, nanorods, nanocubes, nanopyramids, nanoshells, multi-layer nanoshells and combinations thereof.

74. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe with multiple structures for different plasmonics activation regimes.

75. The method of claim 74, wherein the plasmonics activation regime is NIR and/or X rays.

76. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe and the method uses metal nanosystems with the PA.

77. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe and the method uses a combination of semiconductor systems with the PA.

78. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe and the method uses XEOL systems with the PA.

79. The method of claim 68, wherein the plasmonics-active agent is a PEPST probe and the method uses metal nanosystems with the energy modulation agent and the PA.

80. The method of claim 68, wherein the plasmonics-active agent is a PEPST probe and the method uses a combination of semiconductor systems with the energy modulation agent and the PA.

81. The method of claim 68, wherein the plasmonics-active agent is a PEPST probe and the method uses XEOL systems with the energy modulation agent and the PA.

82. The method of claim 68, wherein the plasmonics-active agent is a PEPST probe and the method uses X rays.

83. The method of claim 68, wherein the plasmonics-active agent is a PEPST probe and the method uses X rays.

84. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe comprising plasmonics-active metal nanostructures and the method uses X ray to excite surface plasmons in nanoparticles or subnanoparticles of metal of the plasmonics-active metal nanostructures.

85. The method of claim 66, wherein the plasmonics agent-active is a PEPST probe and the method uses bioreceptors.

86. The method of claim 68, wherein the plasmonics agent-active is a PEPST probe and the method uses bioreceptors.

87. The method of claim 68, wherein the plasmonics-active agent is a PEPST probe and the method uses targeted delivery systems with energy modulation agent-PA systems.

88. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe and the method combines plasmonics photospectral properties, biocompatibility, improved drug payload delivery and passive targeting of metal nanoparticles.

89. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe and the method uses drug delivery and photon radiation or ultrasound to release the PA molecules from antibody systems.

90. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe and the method uses liposomes.

91. The method of claim 68, wherein the plasmonics-active agent is a PEPST probe and the method uses liposomes.

92. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe and the method uses ferritin and/or apoferritin with the PA or an energy modulation agent and the PA.

93. The method of claim 68, wherein the plasmonics-active agent is a PEPST probe and the method uses ferritin and/or apoferritin with the energy modulation agent and the PA.

94. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe and the method uses ultrasound for the PA release and photonic excitation of the PA.

95. The method of claim 68, wherein the plasmonics-active agent is a PEPST probe and the method uses ultrasound for the PA release and photonic excitation of the PA or the energy modulation agent.

96. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe and the method uses multi-photon excitation to activate the at least one activatable pharmaceutical agent.

97. The method of claim 63, wherein the at least one activatable pharmaceutical agent is activated by a multi-photon excitation.

98. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe and the method uses drug delivery, tumor targeting, or drug releasing methods.

99. The method of claim 66, wherein the plasmonics-active agent is a PEPST probe and components of the PEPST probe are bound using conjugations, binding metals to organic and inorganic compounds, and/or biomolecules.

100. The method of claim 68, wherein the plasmonics-active agent is an exciton-induced phototherapy (EIP) probe possessing exciton properties.

101. The method of claim 68, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and which comprises plasmonics-active metal nanostructures, exciton-generating energy modulation agent materials, PA components, with said structures and said materials producing exciton-plasmon coupling (EPC).

102. The method of claim 66, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses a combination of semiconductor systems with the PA.

103. The method of claim 68, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses a combination of semiconductor systems with the energy modulation agent and the PA.

104. The method of claim 66, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses XEOL systems with the PA.

105. The method of claim 68, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses XEOL systems with the energy modulation agent and the PA.

106. The method of claim 66, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses X rays.

107. The method of claim 68, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses X rays.

108. The method of claim 66, wherein the plasmonics agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses bioreceptors.

109. The method of claim 68, wherein the plasmonics agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses bioreceptors.

110. The method of claim 68, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses delivery systems and an energy modulation agent and the PA.

111. The method of claim 66, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method combines EPC properties, biocompatibility, improved drug payload delivery and passive targeting of metal nanoparticles.

112. The method of claim 66, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses drug delivery and photon radiation or ultrasound to release the PA molecules from antibody systems.

113. The method of claim 68, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method combines EPC properties, biocompatibility, improved drug payload delivery and passive targeting of metal nanoparticles.

114. The method of claim 68, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses drug delivery and photon radiation or ultrasound to release the PA molecules from antibody systems.

115. The method of claim 66, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses liposomes.

116. The method of claim 68, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses liposomes.

117. The method of claim 66, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses ferritin and/or apoferritin with the PA.

118. The method of claim 68, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses ferritin and/or apoferritin with the energy modulation agent and/or the PA.

119. The method of claim 66, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses ultrasound for a release and photonic excitation of the PA.

120. The method of claim 68, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses ultrasound for a release and photonic excitation of the energy modulation agent and/or the PA.

121. The method of claim 66, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses a chemically labile-linker for a release and photonic excitation of the PA.

122. The method of claim 68, wherein the plasmonics-active agent is an exciton-plasmon enhanced phototherapy (EPEP) probe and the method uses a chemically labile-linker for a release and photonic excitation of the energy modulation agent and/or the PA.

123. The method of claim 63, wherein said predetermined change modifies the target structure and modulates the biological activity of the target structure thus treating a condition, disorder or disease affecting the target structure.

124. The method of claim 123, wherein said condition, disorder, or disease is mediated by abnormal cellular proliferation and said predetermined change ameliorates the abnormal cellular proliferation.

125. The method of claim 124, wherein said abnormal cellular proliferation is higher than that of cells from a subject not having said condition, disorder or disease.

126. The method of claim 124, wherein said abnormal cellular proliferation is lower than that of cells from a subject not having said condition, disorder or disease.

127. The method of claim 123, wherein said condition, disorder, or disease is not significantly mediated by abnormal cellular proliferation and said predetermined change does not substantially affect cellular proliferation.

128. The method of claim 63, wherein the initiation energy is one of electromagnetic energy, acoustic energy or thermal energy.

129. The method of claim 63, wherein the initiation energy is x-rays, gamma rays, an electron beam, UV radiation, visible light, infrared radiation, microwaves or radio waves.

130. The method of claim 63, wherein the initiation energy has the capability of penetrating completely through the subject.

131. The method of claim 63, wherein the initiation energy source is selected from the group consisting of phosphorescent compounds, chemiluminescent compounds, bioluminescent compounds and light emitting enzymes.

132. The method of claim 123, wherein the condition, disorder, or disease is a cell proliferation disorder that is at least one member selected from the group consisting of cancer, bacterial infection, viral infection, parasitic infection, prion infection, fungal infection, immune rejection response, autoimmune disorders, aplastic conditions, and combinations thereof.

133. The method of claim 123, wherein said condition, disorder, or disease is selected from the group consisting of cardiac ablasion, photoangioplastic conditions, intimal hyperplasia, arteriovenous fistula, macular degeneration, psoriasis, acne, hopecia areata, portwine spots, hair removal, autoimmune diseases, rheumatoid and inflammatory arthritis, behavioral and cognitive disorders/conditions, joint conditions, Parkinson'"'"'s disease, retinal injuries and other ocular diseases, enlarged prostate, varicose veins, reduction or removal of fat deposits (liposuction), nerve regeneration, sensory regeneration/restoration, wound healing, chronic pain, conditions occuring in bone tissue, conditions occuring in a soft tissue and/or cartilage, and lymph node conditions.

134. The method of claim 63, wherein the at least one activatable pharmaceutical agent is a photoactivatable agent.

135. The method of claim 63, wherein the at least one activatable pharmaceutical agent is selected from psoralens, pyrene cholesteryloleate, acridine, porphyrin, fluorescein, rhodamine, 16-diazorcortisone, ethidium, transition metal complexes of bleomycin, transition metal complexes of deglycobleomycin organoplatinum complexes, alloxazines, vitamin Ks, vitamin L, vitamin metabolites, vitamin precursors, naphthoquinones, naphthalenes, naphthols and derivatives thereof having planar molecular conformations, porphorinporphyrins, dyes and phenothiazine derivatives, coumarins, quinolones, quinones, and anthroquinones.

136. The method of claim 135, wherein the at least one activatable pharmaceutical agent is a psoralen, a coumarin, a porphyrin or a derivative thereof.

137. The method of claim 135, wherein the at least one activatable pharmaceutical agent is 8-MOP or AMT.

138. The method of claim 63, wherein the at least one activatable pharmaceutical agent is one selected from 7,8-dimethyl-10-ribityl, isoalloxazine, 7,8,10-trimethylisoalloxazine, 7,8-dimethylalloxazine, isoalloxazine-adenine dinucleotide, alloxazine mononucleotide, aluminum (III) phthalocyanine tetrasulonate, hematophorphyrin, and phthadocyanine.

139. The method of claim 63, wherein the at least one activatable pharmaceutical agent is coupled to a carrier that is capable of binding to a receptor site on or near the target structure.

140. The method of claim 139, wherein the carrier is one selected from insulin, interleukin, thymopoietin or transferrin.

141. The method of claim 139, wherein the at least one activatable pharmaceutical agent is coupled to the carrier by a covalent bond.

142. The method of claim 139, wherein the at least one activatable pharmaceutical agent is coupled to the carrier by non-covalent bond.

143. The method of claim 139, wherein the receptor site is one selected from nucleic acids of nucleated cells, antigenic sites on nucleated cells, or epitopes.

144. The method of claim 63, wherein the at least one activatable pharmaceutical agent has affinity for the target stricture.

145. The method of claim 63, wherein the target structure is a target cell and the at least one activatable pharmaceutical agent is capable of being preferentially absorbed by the target cell.

146. The method of claim 63, wherein the target structure is a target cell and the predetermined change is apoptosis in the target cell.

147. The method of claim 63, wherein the at least one activatable pharmaceutical agent, upon activation, causes an auto-vaccine effect in the subject that reacts with a target structure.

148. The method of claim 63, wherein the at least one activatable pharmaceutical agent is a DNA intercalator or a halogenated derivative thereof.

149. The method of claim 64, wherein said at least one energy modulation agent is a single energy modulation agent.

150. The method of claim 65, wherein said at least one energy modulation agent is a single energy modulation agent.

151. The method of claim 64, wherein said at least one energy modulation agent is a plurality of the energy modulation agents, and wherein the initiation energy is converted, through a cascade energy transfer between the plurality of the energy modulation agents, to an energy that activates the at least one activatable pharmaceutical agent.

152. The method of claim 63, wherein the at least one activatable pharmaceutical agent comprises an active agent contained within a photocage, wherein upon exposure to said initiation energy source, the photocage disassociates from the active agent, rendering the active agent available.

153. The method of claim 64, wherein the at least one activatable pharmaceutical agent comprises an active agent contained within a photocage, wherein upon exposure to a reemitted energy by the at least one energy modulation agent as the activation energy of the at least one activatable pharmaceutical agent, the photocage disassociates from the active agent, rendering the active agent available.

154. The method of claim 63, wherein said predetermined change to the target structure treats a cell proliferation disorder by causing an increase or decrease in cell proliferation rate of a target cell.

155. The method of claim 64, wherein the initiation energy source is a source of lower energy than UV-A, visible energy, or near infrared energy, other than infrared energy, and said at least one energy modulation agent converts the initiation energy to UV-A, visible or near infrared energy.

156. The method of claim 64, wherein if the initiation energy is an infrared energy, the energy activating the activatable agent is not UV or visible light energy.

157. The method of claim 64, wherein the at least one energy modulation agent is one or more members selected from a biocompatible fluorescing metal nanoparticle, fluorescing metal oxide nanoparticle, fluorescing metal coated metal oxide nanoparticle, fluorescing dye molecule, gold nanoparticle, silver nanoparticle, gold-coated silver nanoparticle, a water soluble quantum dot encapsulated by polyamidoamine dendrimers, a luciferase, a biocompatible phosphorescent molecule, a combined electromagnetic energy harvester molecule, and a lanthanide chelate exhibiting intense luminescence.

158. The method of claim 63, wherein the initiation energy is applied via a thin fiber optic.

159. The method of claim 63, further comprising a blocking agent, wherein the blocking agent is capable of blocking uptake of the at least one activatable pharmaceutical agent prior to its activation.

160. The method of claim 159, wherein the target structure is a target cell, and wherein the blocking agent slows down mitosis in non-target cells while allowing target cells to maintain an abnormal rate of mitosis.

161. The method of claim 63, wherein the initiation energy applied and at least one activatable pharmaceutical agent upon activation produce a level of singlet oxygen in the subject that is insufficient to produce cell lysis.

162. The method according to claim 161, wherein the amount of singlet oxygen production is less than 10⁹ singlet oxygen molecules/cell.

163. The method according to claim 162, wherein the amount of singlet oxygen production is less than 0.32×

10<sup>−

3</sup> mol/liter.

164. The method of claim 64, wherein said energy modulation agent is specifically located around, on, or in said target structure.

165. The method of claim 63, in which said predetermined change results in destruction or inactivation of the target structure.

166. The method of claim 63, in which said predetermined change does not result in destruction or inactivation of the target structure.

167. The method of claim 63, wherein the target structure is a eukaryotic cell.

168. The method of claim 63, wherein the target structure is a prokaryotic cell.

169. The method of claim 63, wherein the target structure is a subcellular structure, such as the cell membrane, mitochondria, cell nucleus, or other cell organelle.

170. The method of claim 63, wherein the target structure is an extracellular structure.

171. The method of claim 63, wherein the target structure is a virus or prion.

172. The method of claim 63, wherein the activatable pharmaceutical agent comprises a light-sensitive protein that upon exposure to said initiation energy source modulates a signaling event in the brain.

173. The method of claim 64, wherein the energy modulation agent converts the applied initiation energy to UV-A or visible energy, when then activates the activatable pharmaceutical agent in situ.

174. The method of claim 173, wherein the initiation energy source is a source of higher energy than the resulting UV-A or visible energy.

175. The method of claim 173, wherein the initiation energy source is a source of lower energy than the resulting UV-A or visible energy.

176. The method of claim 63, wherein said predetermined change enhances the expression of, promotes the growth of, or increases the quantity of said target structure.

177. The method of claim 63, wherein said predetermined change enhances, inhibits or stabilizes the usual biological activity of said target structure compared to a similar untreated target structure.

178. The method of claim 63, wherein said predetermined change alters the immunological or chemical properties of said target structure.

179. The method of claim 178, wherein said target structure is a compound that is modified by said predetermined change to be more or less antigenic or immunogenic.

180. The method of claim 68, comprising applying the initiation energy to the at least one energy modulation agent and/or exciton-generating energy modulation agent which modifies the initiation energy into an energy which is enhanced by the at least one plasmonics-active agent.

181. The method of claim 68, wherein the at least one energy modulation agent and/or exciton-generating energy modulation agent modifies the energy enhanced by the plasmonics-active agent, such that the modified energy activates the activatable pharmaceutical agent.

182. The method of claim 69, comprising applying the initiation energy to the at least one energy modulation agent and/or exciton-generating energy modulation agent which modifies the initiation energy into an energy which is enhanced by the at least one plasmonics-active agent.

183. The method of claim 69, wherein the at least one energy modulation agent and/or exciton-generating energy modulation agent modifies the energy enhanced by the plasmonics-active agent, such that the modified energy activates the activatable pharmaceutical agent.

184. The method of claim 63, wherein said initiation energy source is a chemical energy source.

185. The method of claim 64, further comprising administering to the subject nanotubes configured to receive and transmit radiowaves, wherein the initiation energy is radiowaves, and wherein said radiowaves are accepted by said at least one energy modulation agent and transformed into an energy that activates said at least one activatable pharmaceutical agent.

186. A method for treating a condition, disorder, or disease mediated by a target structure in a subject, comprising:

a. modifying one or more cells to incorporate a photon emitting modification or substance;

b. inserting the modified cells at a targeted site of the subject; and

c. administering at least one activatable pharmaceutical agent capable of being activated by the photons emitted from the modified cells to cause a predetermined change to the target structure.

187. The method of claim 186, wherein said one or more cells are subject'"'"'s own cells that have been removed prior to said modifying.

188. The method of claim 186, wherein the photon emitting modification or substance is a member selected from the group consisting of light emitting genes;

phosphorescent compounds, chemiluminescent compounds, bioluminescent compounds and light emitting enzymes.

189. The method of claim 186, wherein the targeted site is a tumor.

190. The method according to claim 186, wherein the at least one activatable pharmaceutical agent, upon activation, causes an auto-vaccine effect in the subject that reacts with a target cell.

191. The method of claim 186, wherein the predetermined change to the target structure induces apoptosis in a target cell.

192. A computer-implemented system, comprising:

a central processing unit (CPU) having a storage medium on which is provided;

a database of excitable compounds;

a first computation module for identifying and designing an excitable compound that is capable of binding with a target cellular structure or component; and

a second computation module predicting the resonance absorption energy of the excitable compound,

wherein the system, upon selection of a target cellular structure or component, computes an excitable compound that is capable of binding with the target structure followed by a computation to predict the resonance absorption energy of the excitable compound.

193. The computer implemented system of claim 192, further comprising an energy initiation source connected to the CPU, wherein after computation of the resonance absorption energy of the excitable compound, the system directs the energy initiation source to provide the computed resonance absorption energy to the excitable compound.

194. A kit for modifying a target structure which mediates or is associated with a biological activity, comprising:

at least one agent selected from the group consisting of energy modulation agents, plasmonics-active agents and combinations thereof;

wherein the energy modulation agent, if present, upgrades or downgrades an initiation energy to an activation energy capable of causing, either directly or indirectly, a predetermined change in the target structure;

wherein the plasmonics-active agent, if present, enhances or modifies the applied initiation energy or the activation energy generated by the energy modulation agent, or both; and

one or more containers suitable for storing the agents in stable forms.

195. The kit of claim 194, further comprising instructions for administering the at least one agent to a subject.

196. The kit of claim 194, wherein the at least one agent comprises at least one energy modulation agent, wherein the at least one energy modulation agent is one or more members selected from a biocompatible fluorescing metal nanoparticle, fluorescing metal oxide nanoparticle, fluorescing metal coated metal oxide nanoparticle, fluorescing dye molecule, gold nanoparticle, silver nanoparticle, gold-coated silver nanoparticle, a water soluble quantum dot encapsulated by polyamidoamine dendrimers, a luciferase, a biocompatible phosphorescent molecule, a combined electromagnetic energy harvester molecule, and a lanthanide chelate exhibiting intense luminescence.

197. The kit of claim 194, further comprising at least one activatable pharmaceutical agent.

198. The kit of claim 197, further comprising instructions for administering the at least one activatable pharmaceutical agent and at least one agent selected from the group consisting of energy modulation agents, plasmonics-active agents and combinations thereof, to a subject and for activating the at least one activatable pharmaceutical agent by application of an initiation energy.

199. The kit of claim 197, wherein the at least one activatable pharmaceutical agent is a photoactivatable agent.

200. The kit of claim 197, wherein the at least one activatable pharmaceutical agent is selected from psoralens, pyrene cholesteryloleate, acridine, porphyrin, fluorescein, rhodamine, 16-diazorcortisone, ethidium, transition metal complexes of bleomycin, transition metal complexes of deglycobleomycin organoplatinum complexes, alloxazines, vitamin Ks, vitamin L, vitamin metabolites, vitamin precursors, naphthoquinones, naphthalenes, naphthols and derivatives thereof having planar molecular conformations, porphorinporphyrins, dyes and phenothiazine derivatives, coumarins, quinolones, quinones, and anthroquinones.

201. The kit of claim 197, wherein the at least one activatable pharmaceutical agent is a psoralen, a coumarin, a porphyrin or a derivative thereof.

202. The kit of claim 197, wherein the at least one activatable pharmaceutical agent is 8-MOP or AMT.

203. The kit of claim 197, wherein the at least one activatable pharmaceutical agent is one selected from 7,8-dimethyl-10-ribityl, isoalloxazine, 7,8,10-trimethylisoalloxazine, 7,8-dimethylalloxazine, isoalloxazine-adenine dinucleotide, alloxazine mononucleotide, aluminum (III) phthalocyanine tetrasulonate, hematophorphyrin, and phthadocyanine.

204. The kit of claim 197, wherein the at least one activatable pharmaceutical agent is coupled to a carrier that is capable of binding to a receptor site on or near the target structure.

205. The kit of claim 204, wherein the carrier is one selected from insulin, interleukin, thymopoietin or transferrin.

206. The kit of claim 204, wherein the at least one activatable pharmaceutical agent is coupled to the carrier by a covalent bond.

207. The kit of claim 204, wherein the at least one activatable pharmaceutical agent is coupled to the carrier by non-covalent bond.

208. The kit of claim 204, wherein the receptor site is one selected from nucleic acids of nucleated cells, antigenic sites on nucleated cells, or epitopes.

209. The kit of claim 197, wherein the at least one activatable pharmaceutical agent has affinity for the target structure.

210. The kit of claim 197, wherein the target structure is a target cell and the at least one activatable pharmaceutical agent is capable of being preferentially absorbed by the target cell.

211. The kit of claim 194, wherein the target structure is a target cell and the predetermined change is apoptosis in the target cell.

212. The kit of claim 197, wherein the at least one activatable pharmaceutical agent, upon activation, causes an auto-vaccine effect in the subject that reacts with a target structure.

213. The kit of claim 197, wherein the at least one activatable pharmaceutical agent is a DNA intercalator or a halogenated derivative thereof.

214. The kit of claim 194, wherein the at least one agent is at least one energy modulation agent.

215. The kit of claim 214, wherein the at least one energy modulation agent is a single energy modulation agent.

216. The kit of claim 214, wherein said at least one energy modulation agent is a plurality of the energy modulation agents, and wherein the initiation energy is converted, through a cascade energy transfer between the plurality of the energy modulation agents, to the activation energy.

217. The kit of claim 197, wherein the at least one activatable pharmaceutical agent comprises an active agent contained within a photocage, wherein upon exposure to an initiation energy source, the photocage disassociates from the active agent, rendering the active agent available.

218. The kit of claim 197, wherein the at least one activatable pharmaceutical agent comprises an active agent contained within a photocage, wherein upon exposure to a reemitted energy by the at least one energy modulation agent as an activation energy of the at least one activatable pharmaceutical agent, the photocage disassociates from the active agent, rendering the active agent available.

219. The kit of claim 214, wherein said at least one energy modulation agent is a single energy modulation agent, and is coupled to at least one activatable pharmaceutical agent.

220. The kit of claim 214, comprising a plurality of energy modulation agents, capable of converting, through a cascade energy transfer between the plurality of energy modulation agents, the initiation energy to an activation energy that activates at least one activatable pharmaceutical agent.

221. The kit of claim 194, wherein the at least one agent is at least one plasmonics-active agent.

222. The kit of claim 194, wherein the at least one agent is a combination of at least one energy modulation agent and at least one plasmonics-active agent.

223. The kit of claim 221, wherein the at least one plasmonics-active agent is a PEPST probe with multi plasmonics resonance mode.

224. The kit of claim 221, wherein the plasmonics-active agent is a PEPST probe comprising plasmonics-active metal nanostructures.

225. The kit of claim 224, wherein the metal nanostructures are nanospheres, nanorods, nanocubes, nanopyramids, nanoshells, multi-layer nanoshells and combinations thereof.

226. The kit of claim 221, wherein the plasmonics-active agent is a PEPST probe with multiple structures for different plasmonics activation regimes.

227. The kit of claim 226, wherein the plasmonics activation regime is NIR and/or X rays.

228. The kit of claim 221, wherein the plasmonics-active agent is an exciton-induced phototherapy (EIP) probe possessing exciton properties.

229. The kit of claim 222, wherein the at least one plasmonics-active agent is a PEPST probe with multi plasmonics resonance mode.

230. The kit of claim 222, wherein the plasmonics-active agent is a PEPST probe comprising plasmonics-active metal nanostructures.

231. The kit of claim 230, wherein the metal nanostructures are nanospheres, nanorods, nanocubes, nanopyramids, nanoshells, multi-layer nanoshells and combinations thereof.

232. The kit of claim 222, wherein the plasmonics-active agent is a PEPST probe with multiple structures for different plasmonics activation regimes.

233. The kit of claim 232, wherein the plasmonics activation regime is NIR and/or X rays.

234. The kit of claim 222, wherein the plasmonics-active agent is an exciton-induced phototherapy (EIP) probe possessing exciton properties.

235. The kit of claim 221, further comprising at least one activatable pharmaceutical agent.

236. The kit of claim 222, further comprising at least one activatable pharmaceutical agent.

237. A pharmaceutical composition for modifying a target structure which mediates or is associated with a biological activity, comprising:

at least one agent selected from the group consisting of energy modulation agents, plasmonics-active agents and combinations thereof; and

a pharmaceutically acceptable carrier.

238. The pharmaceutical composition of claim 237, further comprising a chemical energy source.

239. The pharmaceutical composition of claim 238, wherein the chemical energy source is a member selected from the group consisting of phosphorescent compounds, chemiluminescent compounds, bioluminescent compounds and light emitting enzymes.

240. The pharmaceutical composition of claim 237, wherein the at least one agent comprises at least one energy modulation agent, wherein the at least one energy modulation agent is one or more members selected from a biocompatible fluorescing metal nanoparticle, fluorescing metal oxide nanoparticle, fluorescing metal coated metal oxide nanoparticle, fluorescing dye molecule, gold nanoparticle, silver nanoparticle, gold-coated silver nanoparticle, a water soluble quantum dot encapsulated by polyamidoamine dendrimers, a luciferase, a biocompatible phosphorescent molecule, a combined electromagnetic energy harvester molecule, and a lanthanide chelate exhibiting intense luminescence.

241. The pharmaceutical composition of claim 237, further comprising at least one activatable pharmaceutical agent.

242. The pharmaceutical composition of claim 241, wherein the at least one activatable pharmaceutical agent is a photoactivalable agent.

243. The pharmaceutical composition of claim 241, wherein the at least one activatable pharmaceutical agent is selected from psoralens, pyrene cholesteryloleate, acridine, porphyrin, fluorescein, rhodamine, 16-diazorcortisone, ethidium, transition metal complexes of bleomycin, transition metal complexes of deglycobleomycin organoplatinum complexes, alloxazines, vitamin Ks, vitamin L, vitamin metabolites, vitamin precursors, naphthoquinones, naphthalenes, naphthols and derivatives thereof having planar molecular conformations, porphorinporphyrins, dyes and phenothiazine derivatives, coumarins, quinolones, quinones, and anthroquinones.

244. The pharmaceutical composition of claim 241, wherein the at least one activatable pharmaceutical agent is a psoralen, a coumarin, a porphyrin or a derivative thereof.

245. The pharmaceutical composition of claim 241, wherein the at least one activatable pharmaceutical agent is 8-MOP or AMT.

246. The pharmaceutical composition of claim 241, wherein the at least one activatable pharmaceutical agent is one selected from 7,8-dimethyl-10-ribityl, isoalloxazine, 7,8,10-trimethylisoalloxazine, 7,8-dimethylalloxazine, isoalloxazine-adenine dinucleotide, alloxazine mononucleotide, aluminum (III) phthalocyanine tetrasulonate, hematophorphyrin, and phthadocyanine.

247. The pharmaceutical composition of claim 241, wherein the at least one activatable pharmaceutical agent is coupled to a carrier that is capable of binding to a receptor site on or near the target structure.

248. The pharmaceutical composition of claim 247, wherein the carrier is one selected from insulin, interleukin, thymopoietin or transferrin.

249. The pharmaceutical composition of claim 247, wherein the at least one activatable pharmaceutical agent is coupled to the carrier by a covalent bond.

250. The pharmaceutical composition of claim 247, wherein the at least one activatable pharmaceutical agent is coupled to the carrier by non-covalent bond.

251. The pharmaceutical composition of claim 247, wherein the receptor site is one selected from nucleic acids of nucleated cells, antigenic sites on nucleated cells, or epitopes.

252. The pharmaceutical composition of claim 247, wherein the at least one activatable pharmaceutical agent has affinity for the target structure.

253. The pharmaceutical composition of claim 252, wherein the target structure is a target cell and the at least one activatable pharmaceutical agent is capable of being preferentially absorbed by the target cell.

254. The pharmaceutical composition of claim 241, wherein the target structure is a target cell and the predetermined change is apoptosis in the target cell.

255. The pharmaceutical composition of claim 252, wherein the at least one activatable pharmaceutical agent, upon activation, causes an auto-vaccine effect in the subject that reacts with a target structure.

256. The pharmaceutical composition of claim 241, wherein the at least one activatable pharmaceutical agent is a DNA intercalator or a halogenated derivative thereof.

257. The pharmaceutical composition of claim 237, wherein the at least one agent is at least one energy modulation agent.

258. The pharmaceutical composition of claim 257, wherein the at least one energy modulation agent is a single energy modulation agent.

259. The pharmaceutical composition of claim 257, wherein said at least one energy modulation agent is a plurality of the energy modulation agents, and wherein an initiation energy is converted, through a cascade energy transfer between the plurality of the energy modulation agents, to an activation energy which effects the modifying of the target structure.

260. The pharmaceutical composition of claim 241, wherein the at least one activatable pharmaceutical agent comprises an active agent contained within a photocage, wherein upon exposure to an initiation energy source, the photocage disassociates from the active agent, rendering the active agent available.

261. The pharmaceutical composition of claim 241, wherein the at least one activatable pharmaceutical agent comprises an active agent contained within a photocage, wherein upon exposure to a reemitted energy by the at least one energy modulation agent as an activation energy of the at least one activatable pharmaceutical agent, the photocage disassociates from the active agent, rendering the active agent available.

262. The pharmaceutical composition of claim 257, wherein said at least one energy modulation agent is a single energy modulation agent, and is coupled to at least one activatable pharmaceutical agent.

263. The pharmaceutical composition of claim 257, wherein said at least one energy modulation agent is a plurality of energy modulation agents, capable of converting, through a cascade energy transfer between the plurality of energy modulation agents, an initiation energy to an activation energy that activates at least one activatable pharmaceutical agent.

264. The pharmaceutical composition of claim 237, wherein the at least one agent is at least one plasmonics-active agent.

265. The pharmaceutical composition of claim 237, wherein the at least one agent is a combination of at least one energy modulation agent and at least one plasmonics-active agent.

266. The pharmaceutical composition of claim 264, wherein the at least one plasmonics-active agent is a PEPST probe with multi plasmonics resonance mode.

267. The pharmaceutical composition of claim 264, wherein the plasmonics-active agent is a PEPST probe comprising plasmonics-active metal nanostructures.

268. The pharmaceutical composition of claim 267, wherein the metal nanostructures are nanospheres, nanorods, nanocubes, nanopyramids, nanoshells, multi-layer nanoshells and combinations thereof.

269. The pharmaceutical composition of claim 264, wherein the plasmonics-active agent is a PEPST probe with multiple structures for different plasmonics activation regimes.

270. The pharmaceutical composition of claim 269, wherein the plasmonics activation regime is NIR and/or X rays.

271. The pharmaceutical composition of claim 264, wherein the plasmonics-active agent is an exciton-induced phototherapy (EIP) probe possessing exciton properties.

272. The pharmaceutical composition of claim 265, wherein the at least one plasmonics-active agent is a PEPST probe with multi plasmonics resonance mode.

273. The pharmaceutical composition of claim 265, wherein the plasmonics-active agent is a PEPST probe comprising plasmonics-active metal nanostructures.

274. The pharmaceutical composition of claim 273, wherein the metal nanostructures are nanospheres, nanorods, nanocubes, nanopyramids, nanoshells, multi-layer nanoshells and combinations thereof.

275. The pharmaceutical composition of claim 265, wherein the plasmonics-active agent is a PEPST probe with multiple structures for different plasmonics activation regimes.

276. The pharmaceutical composition of claim 275, wherein the plasmonics activation regime is NIR and/or X rays.

277. The pharmaceutical composition of claim 265, wherein the plasmonics-active agent is an exciton-induced phototherapy (EIP) probe possessing exciton properties.

278. The pharmaceutical composition of claim 264, further comprising at least one activatable pharmaceutical agent.

279. The pharmaceutical composition of claim 237, further comprising at least one activatable pharmaceutical agent.

280. The pharmaceutical composition of claim 279, wherein the at least one activatable pharmaceutical agent is a photoactivatable agent.

281. The pharmaceutical composition of claim 279, wherein the at least one activatable pharmaceutical agent is selected from psoralens, pyrene cholesteryloleate, acridine, porphyrin, fluorescein, rhodamine, 16-diazorcortisone, ethidium, transition metal complexes of bleomycin, transition metal complexes of deglycobleomycin organoplatinum complexes, alloxazines, vitamin Ks, vitamin L, vitamin metabolites, vitamin precursors, naphthoquinones, naphthalenes, naphthols and derivatives thereof having planar molecular conformations, porphorinporphyrins, dyes and phenothiazine derivatives, coumarins, quinolones, quinones, and anthroquinones.

282. The pharmaceutical composition of claim 279, wherein the at least one activatable pharmaceutical agent is a psoralen, a coumarin, a porphyrin or a derivative thereof.

283. The pharmaceutical composition of claim 279, wherein the at least one activatable pharmaceutical agent is 8-MOP or AMT.

284. The pharmaceutical composition of claim 279, wherein the at least one activatable pharmaceutical agent is one selected from 7,8-dimethyl-10-ribityl, isoalloxazine, 7,8,10-trimethylisoalloxazine, 7,8-dimethylalloxazine, isoalloxazine-adenine dinucleotide, alloxazine mononucleotide, aluminum (III) phthalocyanine tetrasulonate, hematophorphyrin, and phthadocyanine.

285. The pharmaceutical composition of claim 279, wherein the at least one activatable pharmaceutical agent is coupled to a carrier that is capable of binding to a receptor site on or near the target structure.

286. The pharmaceutical composition of claim 285, wherein the carrier is one selected from insulin, interleukin, thymopoietin or transferrin.

287. The pharmaceutical composition of claim 285, wherein the at least one activatable pharmaceutical agent is coupled to the carrier by a covalent bond.

288. The pharmaceutical composition of claim 285, wherein the at least one activatable pharmaceutical agent is coupled to the carrier by non-covalent bond.

289. The pharmaceutical composition of claim 285, wherein the receptor site is one selected from nucleic acids of nucleated cells, antigenic sites on nucleated cells, or epitopes.

290. The pharmaceutical composition of claim 279, wherein the at least one activatable pharmaceutical agent has affinity for the target structure.

291. The pharmaceutical composition of claim 290, wherein the target structure is a target cell and the at least one activatable pharmaceutical agent is capable of being preferentially absorbed by the target cell.

292. The pharmaceutical composition of claim 279, wherein the target structure is a target cell and the predetermined change is apoptosis in the target cell.

293. The pharmaceutical composition of claim 279, wherein the at least one activatable pharmaceutical agent, upon activation, causes an auto-vaccine effect in the subject that reacts with a target structure.

294. The pharmaceutical composition of claim 279, wherein the at least one activatable pharmaceutical agent is a DNA intercalator or a halogenated derivative thereof.

295. The pharmaceutical composition of claim 279, wherein the at least one activatable pharmaceutical agent comprises an active agent contained within a photocage, wherein upon exposure to an initiation energy source, the photocage disassociates from the active agent, rendering the active agent available.

296. The pharmaceutical composition of claim 279, wherein the at least one activatable pharmaceutical agent comprises an active agent contained within a photocage, wherein upon exposure to a reemitted energy by the at least one energy modulation agent as an activation energy of the at least one activatable pharmaceutical agent, the photocage disassociates from the active agent, rendering the active agent available.

297. The pharmaceutical composition of claim 237, further comprising at least one additive having a complementary therapeutic or diagnostic effect, wherein said additive is at least one member selected from the group consisting of antioxidants, adjuvants, chemical energy sources, and combinations thereof.